Cytoplasmic proteins that specifically bind MINERALOCORTICOIDS and mediate their cellular effects. The receptor with its bound ligand acts in the nucleus to induce transcription of specific segments of DNA.
A group of CORTICOSTEROIDS primarily associated with water and electrolyte balance. This is accomplished through the effect on ION TRANSPORT in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by PLASMA VOLUME, serum potassium, and ANGIOTENSIN II.
Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.
A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827)
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
An high-affinity, NAD-dependent 11-beta-hydroxysteroid dehydrogenase that acts unidirectionally to catalyze the dehydrogenation of CORTISOL to CORTISONE. It is found predominantly in mineralocorticoid target tissues such as the KIDNEY; COLON; SWEAT GLANDS; and the PLACENTA. Absence of the enzyme leads to a fatal form of childhood hypertension termed, APPARENT MINERALOCORTICOID EXCESS SYNDROME.
A hereditary disease characterized by childhood onset HYPERTENSION, hypokalemic alkalosis, and low RENIN and ALDOSTERONE secretion. It results from a defect in the activity of the 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE 2 enzyme which results in inadequate conversion of CORTISOL to CORTISONE. The build up of unprocessed cortisol to levels that stimulate MINERALOCORTICOID RECEPTORS creates the appearance of having excessive MINERALOCORTICOIDS.
A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.
Hydroxysteroid dehydrogenases that catalyzes the reversible conversion of CORTISOL to the inactive metabolite CORTISONE. Enzymes in this class can utilize either NAD or NADP as cofactors.
A synthetic mineralocorticoid with anti-inflammatory activity.
Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.
Cytoplasmic proteins that specifically bind glucocorticoids and mediate their cellular effects. The glucocorticoid receptor-glucocorticoid complex acts in the nucleus to induce transcription of DNA. Glucocorticoids were named for their actions on blood glucose concentration, but they have equally important effects on protein and fat metabolism. Cortisol is the most important example.
A synthetic pregnadiene derivative with anti-aldosterone activity.
Excision of one or both adrenal glands. (From Dorland, 28th ed)
An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1437)
A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.
A mitochondrial cytochrome P450 enzyme that catalyzes the 18-hydroxylation of steroids in the presence of molecular oxygen and NADPH-specific flavoprotein. This enzyme, encoded by CYP11B2 gene, is important in the conversion of CORTICOSTERONE to 18-hydroxycorticosterone and the subsequent conversion to ALDOSTERONE.
A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.
The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.
Sodium channels found on salt-reabsorbing EPITHELIAL CELLS that line the distal NEPHRON; the distal COLON; SALIVARY DUCTS; SWEAT GLANDS; and the LUNG. They are AMILORIDE-sensitive and play a critical role in the control of sodium balance, BLOOD VOLUME, and BLOOD PRESSURE.
Straight tubes commencing in the radiate part of the kidney cortex where they receive the curved ends of the distal convoluted tubules. In the medulla the collecting tubules of each pyramid converge to join a central tube (duct of Bellini) which opens on the summit of the papilla.
A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.
An anti-inflammatory 9-fluoro-glucocorticoid.
An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.
Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
A heterogeneous group of disorders characterized by renal electrolyte transport dysfunctions. Congenital forms are rare autosomal disorders characterized by neonatal hypertension, HYPERKALEMIA, increased RENIN activity and ALDOSTERONE concentration. The Type I features HYPERKALEMIA with sodium wasting; Type II, HYPERKALEMIA without sodium wasting. Pseudohypoaldosteronism can be the result of a defective renal electrolyte transport protein or acquired after KIDNEY TRANSPLANTATION.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Sodium chloride used in foods.
A naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver to the active metabolite HYDROCORTISONE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)
Tetrahydrocortisol is a metabolite of cortisol, a glucocorticoid hormone produced by the adrenal gland, which is used as a clinical marker to help diagnose conditions such as Cushing's syndrome and congenital adrenal hyperplasia.
A mitochondrial cytochrome P450 enzyme that catalyzes the 11-beta-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11B1 gene, is important in the synthesis of CORTICOSTERONE and HYDROCORTISONE. Defects in CYP11B1 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
11 beta,18,21-Trihydroxypregn-4-ene-3,20-dione.
17,21-Dihydroxypregn-4-ene-3,20-dione. A 17-hydroxycorticosteroid with glucocorticoid and anti-inflammatory activities.
A low-affinity 11 beta-hydroxysteroid dehydrogenase found in a variety of tissues, most notably in LIVER; LUNG; ADIPOSE TISSUE; vascular tissue; OVARY; and the CENTRAL NERVOUS SYSTEM. The enzyme acts reversibly and can use either NAD or NADP as cofactors.
A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.
Proteins found usually in the cytoplasm or nucleus that specifically bind steroid hormones and trigger changes influencing the behavior of cells. The steroid receptor-steroid hormone complex regulates the transcription of specific genes.
A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
Tetrahydrocortisone is a weak, endogenous glucocorticoid hormone, specifically a 3α,17,21-trihydroxy-5β-pregnane, that is synthesized in the adrenal gland from tetrahydrocortisol and further metabolized in the liver.
An agent derived from licorice root. It is used for the treatment of digestive tract ulcers, especially in the stomach. Antidiuretic side effects are frequent, but otherwise the drug is low in toxicity.
The portion of renal tubule that begins from the enlarged segment of the ascending limb of the LOOP OF HENLE. It reenters the KIDNEY CORTEX and forms the convoluted segments of the distal tubule.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).
Androstanes and androstane derivatives which are substituted in any position with one or more hydroxyl groups.
A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.
Substances that dissociate into two or more ions, to some extent, in water. Solutions of electrolytes thus conduct an electric current and can be decomposed by it (ELECTROLYSIS). (Grant & Hackh's Chemical Dictionary, 5th ed)
Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
Metabolites or derivatives of PROGESTERONE with hydroxyl group substitution at various sites.
A non-steroidal anti-inflammatory drug. Oxyphenbutazone eyedrops have been used abroad in the management of postoperative ocular inflammation, superficial eye injuries, and episcleritis. (From AMA, Drug Evaluations Annual, 1994, p2000) It had been used by mouth in rheumatic disorders such as ankylosing spondylitis, osteoarthritis, and rheumatoid arthritis but such use is no longer considered justified owing to the risk of severe hematological adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p27)
Adrenal cortex hormones are steroid hormones produced by the outer portion of the adrenal gland, consisting of glucocorticoids, mineralocorticoids, and androgens, which play crucial roles in various physiological processes such as metabolism regulation, stress response, electrolyte balance, and sexual development and function.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A group of corticosteroids carrying hydroxy groups, usually in the 11- or 17-positions. They comprise the bulk of the corticosteroids used systemically. As they are relatively insoluble in water, salts of various esterified forms are often used for injections or solutions.
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
Unsaturated androstane derivatives which are substituted with two hydroxy groups in any position in the ring system.
A subclass of symporters found in KIDNEY TUBULES, DISTAL that are the major pathway for salt resorption. Inhibition of these symporters by BENZOTHIADIAZINES is the basis of action of some DIURETICS.
A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.
Excess production of ADRENAL CORTEX HORMONES such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE. Hyperadrenal syndromes include CUSHING SYNDROME; HYPERALDOSTERONISM; and VIRILISM.
A collection of NEURONS, tracts of NERVE FIBERS, endocrine tissue, and blood vessels in the HYPOTHALAMUS and the PITUITARY GLAND. This hypothalamo-hypophyseal portal circulation provides the mechanism for hypothalamic neuroendocrine (HYPOTHALAMIC HORMONES) regulation of pituitary function and the release of various PITUITARY HORMONES into the systemic circulation to maintain HOMEOSTASIS.
Sodium or sodium compounds used in foods or as a food. The most frequently used compounds are sodium chloride or sodium glutamate.
A ubiquitous sodium salt that is commonly used to season food.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).
The interactions between the anterior pituitary and adrenal glands, in which corticotropin (ACTH) stimulates the adrenal cortex and adrenal cortical hormones suppress the production of corticotropin by the anterior pituitary.
Pathological processes of the ADRENAL GLANDS.
The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.
A genus of leguminous herbs or shrubs whose roots yield GLYCYRRHETINIC ACID and its derivative, CARBENOXOLONE.
The balance of fluid in the BODY FLUID COMPARTMENTS; total BODY WATER; BLOOD VOLUME; EXTRACELLULAR SPACE; INTRACELLULAR SPACE, maintained by processes in the body that regulate the intake and excretion of WATER and ELECTROLYTES, particularly SODIUM and POTASSIUM.
Proteins that are coded by immediate-early genes, in the absence of de novo protein synthesis. The term was originally used exclusively for viral regulatory proteins that were synthesized just after viral integration into the host cell. It is also used to describe cellular proteins which are synthesized immediately after the resting cell is stimulated by extracellular signals.
A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705)
A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
An enzyme that catalyzes the active transport system of sodium and potassium ions across the cell wall. Sodium and potassium ions are closely coupled with membrane ATPase which undergoes phosphorylation and dephosphorylation, thereby providing energy for transport of these ions against concentration gradients.
A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)
An oleanolic acid from GLYCYRRHIZA that has some antiallergic, antibacterial, and antiviral properties. It is used topically for allergic or infectious skin inflammation and orally for its aldosterone effects in electrolyte regulation.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The relationship between the dose of an administered drug and the response of the organism to the drug.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.
A water-soluble ester of METHYLPREDNISOLONE used for cardiac, allergic, and hypoxic emergencies.
Inbred rats derived from Sprague-Dawley rats and used for the study of salt-dependent hypertension. Salt-sensitive and salt-resistant strains have been selectively bred to show the opposite genetically determined blood pressure responses to excess sodium chloride ingestion.
Abnormally high potassium concentration in the blood, most often due to defective renal excretion. It is characterized clinically by electrocardiographic abnormalities (elevated T waves and depressed P waves, and eventually by atrial asystole). In severe cases, weakness and flaccid paralysis may occur. (Dorland, 27th ed)
The internal portion of the kidney, consisting of striated conical masses, the renal pyramids, whose bases are adjacent to the cortex and whose apices form prominent papillae projecting into the lumen of the minor calyces.
A selective aromatase inhibitor effective in the treatment of estrogen-dependent disease including breast cancer.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
An order of bottom fishes with short, small, spinous dorsal fins. It is comprised of one family (Batrachoididae) and about 70 species.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.
A melanocortin receptor subtype found primarily in the ADRENAL CORTEX. It shows specificity for ADRENOCORTICOTROPIC HORMONE.
A pathological condition that removes acid or adds base to the body fluids.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
Unstable isotopes of sodium that decay or disintegrate emitting radiation. Na atoms with atomic weights 20-22 and 24-26 are radioactive sodium isotopes.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The consumption of liquids.
Agents that promote the excretion of urine through their effects on kidney function.
A synthetic amino acid that depletes glutathione by irreversibly inhibiting gamma-glutamylcysteine synthetase. Inhibition of this enzyme is a critical step in glutathione biosynthesis. It has been shown to inhibit the proliferative response in human T-lymphocytes and inhibit macrophage activation. (J Biol Chem 1995;270(33):1945-7)
Elements of limited time intervals, contributing to particular results or situations.
An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.

Valine 571 functions as a regional organizer in programming the glucocorticoid receptor for differential binding of glucocorticoids and mineralocorticoids. (1/205)

The glucocorticoid receptor (GR) interacts specifically with glucocorticoids, whereas its closest relative, the mineralocorticoid receptor (MR), interacts with both glucocorticoids and mineralocorticoids, such as aldosterone. To investigate the mechanism underlying the glucocorticoid/mineralocorticoid specificity of the GR, we used a yeast model system to screen for GR ligand-binding domain mutants, substituted with MR residues in the segment 565-574, that can be efficiently activated by aldosterone. In all such increased activity mutants, valine 571 was replaced by methionine, even though most mutants also contained substitutions of other residues with their MR counterparts. Further analysis in yeast and COS-7 cells has revealed that the identity of residue 571 determines the behavior of other MR substituted residues in the 565-574 segment. Generally, MR substitutions in this region are only consistent with aldosterone binding if residue 571 is also replaced with methionine (MR conformation). If residue 571 is valine (GR conformation), most other MR substitution mutants drastically reduce interaction with both mineralocorticoid and glucocorticoid hormones. Based on these functional data, we hypothesize that residue 571 functions as a regional organizer involved in discriminating between glucocorticoid and mineralocorticoid hormones. We have used a molecular model of the GR ligand-binding domain in an attempt to interpret our functional data in structural terms.  (+info)

Levels of mineralocorticoids in whites and blacks. (2/205)

Blacks appear, on average, to retain more Na than whites. A higher production rate of mineralocorticoids could explain the greater Na retention in blacks. Although production of aldosterone has been shown to be lower in blacks, the level of another mineralocorticoid may be increased. Plasma levels of deoxycorticosterone and cortisol were measured in young whites (n=23; age=16.4+/-3.1[SD] years) and young blacks (n=25; age=13.8+/-1.3 years). Blacks had lower plasma levels of renin activity and aldosterone and lower urinary aldosterone excretion rates; thus, they appeared to be representative of blacks that retain additional Na. Plasma deoxycorticosterone levels were lower in blacks than in whites both at baseline (247+/-161 versus 381+/-270 pmol/L, P=0.048) and after stimulation with adrenocorticotropic hormone (822+/-294 versus 1127+/-628 pmol/L at 30 minutes, P=0.047; 925+/-366 versus 1440+/-834 pmol/L at 60 minutes, P=0.013). Cortisol levels were also lower in blacks at baseline (P=0.014) but were not significantly different from levels in whites after stimulation with adrenocorticotropic hormone. In a larger cohort of 407 whites (age=12.0+/-2.9 years) and 247 blacks (age=12.9+/-3.1 years), 18-hydroxycortisol excretion rates were also lower in blacks (P=0. 021). In conclusion, increased Na retention in blacks does not appear to be secondary to increased production of either aldosterone, deoxycorticosterone, cortisol, or 18-hydroxycortisol. A primary renal mechanism may mediate the increase in Na reabsorption in blacks.  (+info)

Glucocorticoids potently block tumour necrosis factor-alpha- and lipopolysaccharide-induced apoptotic cell death in bovine glomerular endothelial cells upstream of caspase 3 activation. (3/205)

1. Endothelial cell damage in glomeruli and kidney arterioles appears to play a pivotal role in glomerular inflammatory diseases. Glomerular endothelial cells, a specialized microvascular cell type involved in the regulation of glomerular ultrafiltration, die by apoptosis in response to tumour necrosis factor-alpha (TNF-alpha), TNF-alpha/basic fibroblast growth factor (bFGF), TNF-alpha/cycloheximide, and bacterial lipopolysaccharide (LPS). Apoptotic cell death is characterized by extensive DNA cleavage, DNA ladder formation, and characteristic morphological alterations. 2. In search for apoptosis-preventing signals, we identified glucocorticoids as potent death preventing factors. Co-treatment of cells with 10 nM dexamethasone and TNF-alpha, TNF-alpha/bFGF, TNF-alpha/cycloheximide, or LPS blocked roughly 90% of apoptotic cell death in glomerular endothelial cells. 3. Similarly to dexamethasone (TNF-alpha- and LPS-induced apoptosis are prevented with IC50 values of 0.8 and 0.9 nM, respectively), other synthetic and natural forms of glucocorticoids, such as fluocinolone, prednisolone, hydrocortisone, and corticosterone potently inhibited cell death with IC50 values of 0.2, 6, 50 and 1000 nM, for TNF-alpha and 0.7, 8, 100 and 500 nM for LPS, respectively. 4. Apart from glucocorticoids, mineralocorticoids such as aldosterone also blocked TNF-alpha/LPS-induced apoptosis (IC50 approximately 500 nM for TNF-alpha and approximately 500 nM for LPS), whereas sex hormones, i. e. beta-estradiol and testosterone remained without effect. 5. The protective effect of glucocorticoids (and mineralocorticoids) required glucocorticoid receptor binding as it could be antagonized by the glucocorticoid receptor antagonist RU-486. Concerning TNF-alpha and LPS signal transduction, we found that dexamethasone efficiently prevented TNF-alpha- and LPS-induced activation of caspase-3-like proteases. Therefore, we postulate inhibitory mechanisms upstream of terminal death pathways.  (+info)

Genetic, biochemical, and clinical studies of patients with A328V or R213C mutations in 11betaHSD2 causing apparent mineralocorticoid excess. (4/205)

Apparent mineralocorticoid excess is a recessively inherited hypertensive syndrome caused by mutations in the 11beta-hydroxysteroid dehydrogenase type 2 gene, which encodes the enzyme normally responsible for converting cortisol to inactive cortisone. Failure to convert cortisol to cortisone in mineralocorticoid-sensitive tissues permits cortisol to bind to and activate mineralocorticoid receptors, causing hypervolemic hypertension. Typically, these patients have increased ratios of cortisol to cortisone and of 5alpha- to 5beta-cortisol metabolites in serum and urine. We have studied 3 patients in 2 families with severe, apparent mineralocorticoid excess and other family members in terms of their genetic, biochemical, and clinical parameters, as well as normal controls. Two brothers were homozygous for an A328V mutation and the third patient was homozygous for an R213C mutation in the 11beta-hydroxysteroid dehydrogenase type 2 gene; both mutations caused a marked reduction in the activity of the encoded enzymes in transfection assays. The steroid profiles of the 7 heterozygotes and 2 other family members studied were completely normal. The results of a novel assay used to distinguish 5alpha- and 5beta-tetrahydrometabolites suggest that 5beta-reductase activity is reduced or inhibited in apparent mineralocorticoid excess. In 1 patient undergoing renal dialysis for chronic renal insufficiency, direct control of salt and water balance completely corrected the hypertension, emphasizing the importance of mineralocorticoid action in this syndrome.  (+info)

Mutants of 11beta-hydroxysteroid dehydrogenase (11-HSD2) with partial activity: improved correlations between genotype and biochemical phenotype in apparent mineralocorticoid excess. (5/205)

Mutations in the kidney isozyme of human 11-hydroxysteroid dehydrogenase (11-HSD2) cause apparent mineralocorticoid excess, an autosomal recessive form of familial hypertension. We studied 4 patients with AME, identifying 4 novel and 3 previously reported mutations in the HSD11B2 (HSD11K) gene. Point mutations causing amino acid substitutions were introduced into a pCMV5/11HSD2 expression construct and expressed in mammalian CHOP cells. Mutations L179R and R208H abolished activity in whole cells. Mutants S180F, A237V, and A328V had 19%, 72%, and 25%, respectively, of the activity of the wild-type enzyme in whole cells when cortisol was used as the substrate and 80%, 140%, and 55%, respectively, of wild-type activity when corticosterone was used as the substrate. However, these mutant proteins were only 0.6% to 5.7% as active as the wild-type enzyme in cell lysates, suggesting that these mutations alter stability of the enzyme. In regression analyses of all AME patients with published genotypes, several biochemical and clinical parameters were highly correlated with mutant enzymatic activity, demonstrated in whole cells, when cortisol was used as the substrate. These included the ratio of urinary cortisone to cortisol metabolites (R(2)=0.648, P<0.0001), age at presentation (R(2)=0.614, P<0.0001), and birth weight (R(2)=0.576, P=0.0004). Approximately 5% conversion of cortisol to cortisone is predicted in subjects with mutations that completely inactivate HSD11B2, suggesting that a low level of enzymatic activity is mediated by another enzyme, possibly 11-HSD1.  (+info)

Steroid disorders in children: congenital adrenal hyperplasia and apparent mineralocorticoid excess. (6/205)

Our research team and laboratories have concentrated on two inherited endocrine disorders, congenital adrenal hyperplasia (CAH) and apparent mineralocorticoid excess, in thier investigations of the pathophysiology of adrenal steroid hormone disorders in children. CAH refers to a family of inherited disorders in which defects occur in one of the enzymatic steps required to synthesize cortisol from cholesterol in the adrenal gland. Because of the impaired cortisol secretion, adrenocorticotropic hormone levels rise due to impairment of a negative feedback system, which results in hyperplasia of the adrenal cortex. The majority of cases is due to 21-hydroxylase deficiency (21-OHD). Owing to the blocked enzymatic step, cortisol precursors accumulate in excess and are converted to potent androgens, which are secreted and cause in utero virilization of the affected female fetus genitalia in the classical form of CAH. A mild form of the 21-OHD, termed nonclassical 21-OHD, is the most common autosomal recessive disorder in humans, and occurs in 1/27 Ashkenazic Jews. Mutations in the CYP21 gene have been identified that cause both classical and nonclassical CAH. Apparent mineralocorticoid excess is a potentially fatal genetic disorder causing severe juvenile hypertension, pre- and postnatal growth failure, and low to undetectable levels of potassium, renin, and aldosterone. It is caused by autosomal recessive mutations in the HSD11B2 gene, which result in a deficiency of 11beta-hydroxysteroid dehydrogenase type 2. In 1998, we reported a mild form of this disease, which may represent an important cause of low-renin hypertension.  (+info)

Regulation of cyclooxygenase-2 (COX-2) in rat renal cortex by adrenal glucocorticoids and mineralocorticoids. (7/205)

Production of prostaglandins involved in renal salt and water homeostasis is modulated by regulated expression of the inducible form of cyclooxygenase-2 (COX-2) at restricted sites in the rat renal cortex. Because inflammatory COX-2 is suppressed by glucocorticoids, and prostaglandin levels in the kidney are sensitive to steroids, the sensitivity of COX expression to adrenalectomy (ADX) was investigated. By 2 weeks after ADX in mature rats, cortical COX-2 immunoreactivity increased 10-fold in the cortical thick ascending limb and macula densa. The constitutive isoform, COX-1, was unchanged. The magnitude of the changes and specificity of COX-2 immunoreactivity were validated by in situ hybridization histochemistry of COX-2 mRNA and Western blot analysis. Increased COX-2 activity (>5-fold) was documented by using a specific COX-2 inhibitor. The COX-2 up-regulation in ADX rats was reversed by replacement therapy with either corticosterone or deoxycorticosterone acetate. In normal rats, inhibition of glucocorticoid receptors with RU486 or mineralocorticoid receptors with spironolactone caused up-regulation of renal cortical COX-2. These results indicate that COX-2 expression in situ is tonically inhibited by adrenal steroids, and COX-2 is regulated by mineralocorticoids as well as glucocorticoids.  (+info)

Steroid hormone receptor expression and action in bone. (8/205)

The skeleton is a complex tissue, and hormonal control of bone remodelling is elaborate. The important role that steroid hormones play in bone cell development and in the maintenance of normal bone architecture is well established, but it is only relatively recently that it has become possible to describe their precise mechanism of action. This review focuses not only on the steroid hormones (oestrogens, corticosteroids, androgens and progesterone), but also on related hormones (vitamin D, thyroid hormone and the retinoids), all of which act via structurally homologous nuclear receptors that form part of the steroid/thyroid receptor superfamily. By examining the actions of all of these hormones in vivo and in vitro, this review gives a general overview of the current understanding of steroid hormone action in bone. In addition, a comprehensive review of steroid hormone receptor expression in bone cells is included. Finally, the role that future developments, such as steroid hormone receptor knockout mice, will play in our understanding of steroid hormone action in bone is considered.  (+info)

Medical Definition:

Mineralocorticoid Receptors (MRs) are a type of nuclear receptor protein that are activated by the binding of mineralocorticoid hormones, such as aldosterone. These receptors are expressed in various tissues and cells, including the kidneys, heart, blood vessels, and brain.

When activated, MRs regulate gene expression related to sodium and potassium homeostasis, water balance, and electrolyte transport. This is primarily achieved through the regulation of ion channels and transporters in the distal nephron of the kidney, leading to increased sodium reabsorption and potassium excretion.

Abnormalities in mineralocorticoid receptor function have been implicated in several diseases, including hypertension, heart failure, and primary aldosteronism.

Mineralocorticoids are a class of steroid hormones that primarily regulate electrolyte and fluid balance in the body. The most important mineralocorticoid is aldosterone, which is produced by the adrenal gland in response to signals from the renin-angiotensin system. Aldosterone acts on the distal tubules and collecting ducts of the nephrons in the kidneys to increase the reabsorption of sodium ions (Na+) and water into the bloodstream, while promoting the excretion of potassium ions (K+) and hydrogen ions (H+) into the urine. This helps maintain blood pressure and volume, as well as ensuring a proper balance of electrolytes in the body. Other mineralocorticoids include cortisol and corticosterone, which have weak mineralocorticoid activity and play a more significant role as glucocorticoids, regulating metabolism and immune response.

Mineralocorticoid receptor antagonists (MRAs) are a class of medications that block the action of aldosterone, a hormone produced by the adrenal glands. Aldosterone helps regulate sodium and potassium balance and blood pressure by binding to mineralocorticoid receptors in the kidneys, heart, blood vessels, and brain.

When aldosterone binds to these receptors, it promotes sodium retention and potassium excretion, which can lead to an increase in blood volume and blood pressure. MRAs work by blocking the binding of aldosterone to its receptors, thereby preventing these effects.

MRAs are primarily used to treat heart failure, hypertension, and kidney disease. By reducing sodium retention and increasing potassium excretion, MRAs can help lower blood pressure, reduce fluid buildup in the body, and improve heart function. Examples of MRAs include spironolactone and eplerenone.

Spironolactone is a prescription medication that belongs to a class of drugs known as potassium-sparing diuretics. It works by blocking the action of aldosterone, a hormone that helps regulate sodium and potassium balance in your body. This results in increased urine production (diuresis) and decreased salt and fluid retention.

Spironolactone is primarily used to treat edema (fluid buildup) associated with heart failure, liver cirrhosis, or kidney disease. It's also prescribed for the treatment of high blood pressure and primary hyperaldosteronism, a condition where the adrenal glands produce too much aldosterone.

Furthermore, spironolactone is used off-label to treat conditions such as acne, hirsutism (excessive hair growth in women), and hormone-sensitive breast cancer in postmenopausal women.

It's important to note that spironolactone can cause increased potassium levels in the blood (hyperkalemia) and should be used with caution in patients with kidney impairment or those taking other medications that affect potassium balance. Regular monitoring of electrolyte levels, including potassium and sodium, is essential during spironolactone therapy.

Aldosterone is a hormone produced by the adrenal gland. It plays a key role in regulating sodium and potassium balance and maintaining blood pressure through its effects on the kidneys. Aldosterone promotes the reabsorption of sodium ions and the excretion of potassium ions in the distal tubules and collecting ducts of the nephrons in the kidneys. This increases the osmotic pressure in the blood, which in turn leads to water retention and an increase in blood volume and blood pressure.

Aldosterone is released from the adrenal gland in response to a variety of stimuli, including angiotensin II (a peptide hormone produced as part of the renin-angiotensin-aldosterone system), potassium ions, and adrenocorticotropic hormone (ACTH) from the pituitary gland. The production of aldosterone is regulated by a negative feedback mechanism involving sodium levels in the blood. High sodium levels inhibit the release of aldosterone, while low sodium levels stimulate its release.

In addition to its role in maintaining fluid and electrolyte balance and blood pressure, aldosterone has been implicated in various pathological conditions, including hypertension, heart failure, and primary hyperaldosteronism (a condition characterized by excessive production of aldosterone).

11-Beta-Hydroxysteroid Dehydrogenase Type 2 (11β-HSD2) is an enzyme that plays a crucial role in the regulation of steroid hormones, particularly cortisol and aldosterone. It is primarily found in tissues such as the kidneys, colon, and salivary glands.

The main function of 11β-HSD2 is to convert active cortisol into inactive cortisone, which helps to prevent excessive mineralocorticoid receptor activation by cortisol. This is important because cortisol can bind to and activate mineralocorticoid receptors, leading to increased sodium reabsorption and potassium excretion in the kidneys, as well as other effects on blood pressure and electrolyte balance.

By converting cortisol to cortisone, 11β-HSD2 helps to protect mineralocorticoid receptors from being overstimulated by cortisol, allowing aldosterone to bind and activate these receptors instead. This is important for maintaining normal blood pressure and electrolyte balance.

Deficiencies or mutations in the 11β-HSD2 enzyme can lead to a condition called apparent mineralocorticoid excess (AME), which is characterized by high blood pressure, low potassium levels, and increased sodium reabsorption in the kidneys. This occurs because cortisol is able to bind to and activate mineralocorticoid receptors in the absence of 11β-HSD2 activity.

Apparent Mineralocorticoid Excess Syndrome (AME) is a rare inherited endocrine disorder characterized by the overproduction of the mineralocorticoid hormone aldosterone or an increased sensitivity to aldosterone at the level of its target organs. This leads to an excessive reabsorption of sodium and water, as well as an increased excretion of potassium in the urine.

The term "apparent" is used because, despite elevated levels of aldosterone, the regulation of aldosterone secretion appears to be normal. In other words, the syndrome is not caused by a primary defect in the adrenal glands, but rather by an inherited mutation that affects the mineralocorticoid receptor or the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2).

The most common form of AME is caused by a mutation in the gene encoding 11β-HSD2, which is normally responsible for converting cortisol to cortisone in the kidney. Cortisol has a higher affinity for the mineralocorticoid receptor than aldosterone, but its effects are usually blocked by 11β-HSD2. In AME, however, the mutation in 11β-HSD2 leads to an accumulation of cortisol in the kidney, which can then bind to and activate the mineralocorticoid receptor, mimicking the effects of aldosterone.

The clinical features of AME include hypertension, hypokalemia (low potassium levels), metabolic alkalosis (an increase in blood pH due to loss of hydrogen ions in the urine), and suppressed plasma renin activity. If left untreated, AME can lead to severe complications such as heart failure, stroke, and kidney damage. Treatment typically involves the use of medications that block the mineralocorticoid receptor or inhibit aldosterone production.

Desoxycorticosterone (also known as desoxycorticosterone or DCZ) is a natural steroid hormone produced by the adrenal gland. It is a weak glucocorticoid and mineralocorticoid, which means it has some effects on blood sugar metabolism and regulates electrolyte and fluid balance in the body.

Desoxycorticosterone is used as a medication in the form of its synthetic acetate ester, desoxycorticosterone acetate (DCA), to treat Addison's disease, a condition in which the adrenal glands do not produce enough steroid hormones. DCA helps to replace the missing mineralocorticoid activity and prevent the symptoms of low blood pressure, dehydration, and electrolyte imbalances associated with Addison's disease.

It is important to note that desoxycorticosterone should only be used under the supervision of a healthcare provider, as it can have significant side effects if not properly monitored.

11-Beta-Hydroxysteroid dehydrogenases (11-β-HSDs) are a group of enzymes that play a crucial role in the metabolism of steroid hormones, particularly cortisol and cortisone, which belong to the class of glucocorticoids. These enzymes exist in two isoforms: 11-β-HSD1 and 11-β-HSD2.

1. 11-β-HSD1: This isoform is primarily located within the liver, adipose tissue, and various other peripheral tissues. It functions as a NADPH-dependent reductase, converting inactive cortisone to its active form, cortisol. This enzyme helps regulate glucocorticoid action in peripheral tissues, influencing glucose and lipid metabolism, insulin sensitivity, and inflammation.
2. 11-β-HSD2: This isoform is predominantly found in mineralocorticoid target tissues such as the kidneys, colon, and salivary glands. It functions as a NAD+-dependent dehydrogenase, converting active cortisol to its inactive form, cortisone. By doing so, it protects the mineralocorticoid receptor from being overstimulated by cortisol, ensuring aldosterone specifically binds and activates this receptor to maintain proper electrolyte and fluid balance.

Dysregulation of 11-β-HSDs has been implicated in several disease states, including metabolic syndrome, type 2 diabetes, hypertension, and psychiatric disorders. Therefore, understanding the function and regulation of these enzymes is essential for developing novel therapeutic strategies to treat related conditions.

Fludrocortisone is a synthetic corticosteroid hormone, specifically a mineralocorticoid. It is often used to treat conditions associated with low levels of corticosteroids, such as Addison's disease. It works by helping the body retain sodium and lose potassium, which helps to maintain fluid balance and blood pressure.

In medical terms, fludrocortisone is defined as a synthetic mineralocorticoid with glucocorticoid activity used in the treatment of adrenogenital syndrome and Addison's disease, and as an adjunct in the treatment of rheumatoid arthritis. It is also used to treat orthostatic hypotension by helping the body retain sodium and water, thereby increasing blood volume and blood pressure.

It is important to note that fludrocortisone can have significant side effects, particularly if used in high doses or for long periods of time. These can include fluid retention, high blood pressure, increased risk of infection, and slowed growth in children. As with any medication, it should be used under the close supervision of a healthcare provider.

Hydroxysteroid dehydrogenases (HSDs) are a group of enzymes that play a crucial role in steroid hormone metabolism. They catalyze the oxidation and reduction reactions of hydroxyl groups on the steroid molecule, which can lead to the activation or inactivation of steroid hormones. HSDs are involved in the conversion of various steroids, including sex steroids (e.g., androgens, estrogens) and corticosteroids (e.g., cortisol, cortisone). These enzymes can be found in different tissues throughout the body, and their activity is regulated by various factors, such as hormones, growth factors, and cytokines. Dysregulation of HSDs has been implicated in several diseases, including cancer, diabetes, and cardiovascular disease.

Glucocorticoid receptors (GRs) are a type of nuclear receptor proteins found inside cells that bind to glucocorticoids, a class of steroid hormones. These receptors play an essential role in the regulation of various physiological processes, including metabolism, immune response, and stress response.

When a glucocorticoid hormone such as cortisol binds to the GR, it undergoes a conformational change that allows it to translocate into the nucleus of the cell. Once inside the nucleus, the GR acts as a transcription factor, binding to specific DNA sequences called glucocorticoid response elements (GREs) located in the promoter regions of target genes. The binding of the GR to the GRE can either activate or repress gene transcription, depending on the context and the presence of co-regulatory proteins.

Glucocorticoids have diverse effects on the body, including anti-inflammatory and immunosuppressive actions. They are commonly used in clinical settings to treat a variety of conditions such as asthma, rheumatoid arthritis, and inflammatory bowel disease. However, long-term use of glucocorticoids can lead to several side effects, including osteoporosis, weight gain, and increased risk of infections, due to the widespread effects of these hormones on multiple organ systems.

Canrenone, also known as canrenoic acid, is a synthetic steroidal compound that is commonly used as a diuretic and antihypertensive agent. It is a derivative of aldosterone, a hormone that regulates sodium and potassium balance in the body, and works by blocking the action of aldosterone on the distal tubules of the kidney. This leads to increased excretion of sodium and water, which helps to reduce blood volume and lower blood pressure.

Canrenone is often prescribed for the treatment of hypertension, edema associated with heart failure, liver cirrhosis, and nephrotic syndrome. It has also been shown to have anti-androgenic effects and has been used off-label in the treatment of hirsutism and acne.

Like other diuretics, canrenone can cause electrolyte imbalances, particularly low potassium levels (hypokalemia), and may interact with other medications that affect potassium levels. It is important for patients taking canrenone to be monitored regularly for changes in electrolyte levels and kidney function.

Adrenalectomy is a surgical procedure in which one or both adrenal glands are removed. The adrenal glands are small, triangular-shaped glands located on top of each kidney that produce hormones such as cortisol, aldosterone, and adrenaline (epinephrine).

There are several reasons why an adrenalectomy may be necessary. For example, the procedure may be performed to treat tumors or growths on the adrenal glands, such as pheochromocytomas, which can cause high blood pressure and other symptoms. Adrenalectomy may also be recommended for patients with Cushing's syndrome, a condition in which the body is exposed to too much cortisol, or for those with adrenal cancer.

During an adrenalectomy, the surgeon makes an incision in the abdomen or back and removes the affected gland or glands. In some cases, laparoscopic surgery may be used, which involves making several small incisions and using specialized instruments to remove the gland. After the procedure, patients may need to take hormone replacement therapy to compensate for the loss of adrenal gland function.

Corticosterone is a hormone produced by the adrenal gland in many animals, including humans. It is a type of glucocorticoid steroid hormone that plays an important role in the body's response to stress, immune function, metabolism, and regulation of inflammation. Corticosterone helps to regulate the balance of sodium and potassium in the body and also plays a role in the development and functioning of the nervous system. It is the primary glucocorticoid hormone in rodents, while cortisol is the primary glucocorticoid hormone in humans and other primates.

Glucocorticoids are a class of steroid hormones that are naturally produced in the adrenal gland, or can be synthetically manufactured. They play an essential role in the metabolism of carbohydrates, proteins, and fats, and have significant anti-inflammatory effects. Glucocorticoids suppress immune responses and inflammation by inhibiting the release of inflammatory mediators from various cells, such as mast cells, eosinophils, and lymphocytes. They are frequently used in medical treatment for a wide range of conditions, including allergies, asthma, rheumatoid arthritis, dermatological disorders, and certain cancers. Prolonged use or high doses of glucocorticoids can lead to several side effects, such as weight gain, mood changes, osteoporosis, and increased susceptibility to infections.

Aldosterone synthase is a steroidogenic enzyme that is primarily responsible for the production of the hormone aldosterone in the adrenal gland. It is encoded by the CYP11B2 gene and is located within the mitochondria of the zona glomerulosa cells in the adrenal cortex.

Aldosterone synthase catalyzes two key reactions in the biosynthesis of aldosterone: the conversion of corticosterone to 18-hydroxycorticosterone and the subsequent conversion of 18-hydroxycorticosterone to aldosterone. These reactions involve the sequential addition of hydroxyl groups at the C18 position of the steroid molecule, which is a critical step in the synthesis of aldosterone.

Aldosterone plays an important role in regulating blood pressure and electrolyte balance by increasing the reabsorption of sodium and water in the distal nephron of the kidney, while promoting the excretion of potassium. Disorders of aldosterone synthase can lead to conditions such as primary hyperaldosteronism, which is characterized by excessive production of aldosterone and can result in hypertension and hypokalemia.

Mifepristone is a synthetic steroid that is used in the medical termination of pregnancy (also known as medication abortion or RU-486). It works by blocking the action of progesterone, a hormone necessary for maintaining pregnancy. Mifepristone is often used in combination with misoprostol to cause uterine contractions and expel the products of conception from the uterus.

It's also known as an antiprogestin or progesterone receptor modulator, which means it can bind to progesterone receptors in the body and block their activity. In addition to its use in pregnancy termination, mifepristone has been studied for its potential therapeutic uses in conditions such as Cushing's syndrome, endometriosis, uterine fibroids, and hormone-dependent cancers.

It is important to note that Mifepristone should be administered under the supervision of a licensed healthcare professional and it is not available over the counter. Also, it has some contraindications and potential side effects, so it's essential to have a consultation with a doctor before taking this medication.

Hydrocortisone is a synthetic glucocorticoid, which is a class of steroid hormones. It is identical to the naturally occurring cortisol, a hormone produced by the adrenal gland that helps regulate metabolism and helps your body respond to stress. Hydrocortisone has anti-inflammatory effects and is used to treat various inflammatory conditions such as allergies, skin disorders, and autoimmune diseases. It works by suppressing the immune system's response to reduce swelling, redness, itching, and other symptoms caused by inflammation.

Hydrocortisone is available in different forms, including oral tablets, topical creams, lotions, gels, and ointments, as well as injectable solutions. The specific use and dosage depend on the condition being treated and the individual patient's medical history and current health status.

As with any medication, hydrocortisone can have side effects, especially when used in high doses or for extended periods. Common side effects include increased appetite, weight gain, mood changes, insomnia, and skin thinning. Long-term use of hydrocortisone may also increase the risk of developing osteoporosis, diabetes, cataracts, and other health problems. Therefore, it is essential to follow your healthcare provider's instructions carefully when using this medication.

Epithelial Sodium Channels (ENaC) are a type of ion channel found in the epithelial cells that line the surface of many types of tissues, including the airways, kidneys, and colon. These channels play a crucial role in regulating sodium and fluid balance in the body by allowing the passive movement of sodium ions (Na+) from the lumen or outside of the cell to the inside of the cell, following their electrochemical gradient.

ENaC is composed of three subunits, alpha, beta, and gamma, which are encoded by different genes. The channel is normally closed and opens in response to various stimuli, such as hormones, neurotransmitters, or changes in osmolarity. Once open, the channel allows sodium ions to flow through, creating a positive charge that can attract chloride ions (Cl-) and water molecules, leading to fluid absorption.

In the kidneys, ENaC plays an essential role in regulating sodium reabsorption in the distal nephron, which helps maintain blood pressure and volume. In the airways, ENaC is involved in controlling the hydration of the airway surface liquid, which is necessary for normal mucociliary clearance. Dysregulation of ENaC has been implicated in several diseases, including hypertension, cystic fibrosis, and chronic obstructive pulmonary disease (COPD).

Collecting kidney tubules, also known as collecting ducts, are the final portion of the renal tubule in the nephron of the kidney. They collect filtrate from the distal convoluted tubules and glomeruli and are responsible for the reabsorption of water and electrolytes back into the bloodstream under the influence of antidiuretic hormone (ADH) and aldosterone. The collecting ducts then deliver the remaining filtrate to the ureter, which transports it to the bladder for storage until urination.

Hyperaldosteronism is a medical condition characterized by the overproduction of aldosterone, a hormone produced by the adrenal glands. Aldosterone helps regulate sodium and potassium balance and blood pressure by promoting sodium retention and potassium excretion in the kidneys.

There are two types of hyperaldosteronism: primary and secondary. Primary hyperaldosteronism is caused by an overproduction of aldosterone from an abnormality within the adrenal gland, such as a tumor (Conn's syndrome) or hyperplasia. Secondary hyperaldosteronism occurs when there is an excess production of renin, a hormone produced by the kidneys, which then stimulates the adrenal glands to produce more aldosterone. This can be caused by various conditions that affect kidney function, such as renal artery stenosis or heart failure.

Symptoms of hyperaldosteronism may include high blood pressure, low potassium levels (hypokalemia), muscle weakness, and frequent urination. Diagnosis typically involves measuring aldosterone and renin levels in the blood, as well as other tests to determine the underlying cause. Treatment depends on the type and cause of hyperaldosteronism but may include medications, surgery, or lifestyle changes.

Dexamethasone is a type of corticosteroid medication, which is a synthetic version of a natural hormone produced by the adrenal glands. It is often used to reduce inflammation and suppress the immune system in a variety of medical conditions, including allergies, asthma, rheumatoid arthritis, and certain skin conditions.

Dexamethasone works by binding to specific receptors in cells, which triggers a range of anti-inflammatory effects. These include reducing the production of chemicals that cause inflammation, suppressing the activity of immune cells, and stabilizing cell membranes.

In addition to its anti-inflammatory effects, dexamethasone can also be used to treat other medical conditions, such as certain types of cancer, brain swelling, and adrenal insufficiency. It is available in a variety of forms, including tablets, liquids, creams, and injectable solutions.

Like all medications, dexamethasone can have side effects, particularly if used for long periods of time or at high doses. These may include mood changes, increased appetite, weight gain, acne, thinning skin, easy bruising, and an increased risk of infections. It is important to follow the instructions of a healthcare provider when taking dexamethasone to minimize the risk of side effects.

18-Hydroxydesoxycorticosterone is a steroid hormone that is produced by the adrenal gland. It is an intermediate in the biosynthesis of aldosterone, which is the major hormone responsible for regulating sodium and potassium balance in the body. 18-Hydroxydesoxycorticosterone itself has minimal biological activity, but it is converted to aldosterone by the enzyme aldosterone synthase.

The medical relevance of 18-Hydroxydesoxycorticosterone lies in its role as a precursor to aldosterone and its potential use as a marker for certain adrenal gland disorders. For example, increased production of 18-Hydroxydesoxycorticosterone has been observed in some cases of primary hyperaldosteronism, which is a condition characterized by excessive aldosterone production leading to high blood pressure and low potassium levels. Measuring the levels of this hormone can help diagnose and manage such conditions.

Hormone antagonists are substances or drugs that block the action of hormones by binding to their receptors without activating them, thereby preventing the hormones from exerting their effects. They can be classified into two types: receptor antagonists and enzyme inhibitors. Receptor antagonists bind directly to hormone receptors and prevent the hormone from binding, while enzyme inhibitors block the production or breakdown of hormones by inhibiting specific enzymes involved in their metabolism. Hormone antagonists are used in the treatment of various medical conditions, such as cancer, hormonal disorders, and cardiovascular diseases.

Sodium is an essential mineral and electrolyte that is necessary for human health. In a medical context, sodium is often discussed in terms of its concentration in the blood, as measured by serum sodium levels. The normal range for serum sodium is typically between 135 and 145 milliequivalents per liter (mEq/L).

Sodium plays a number of important roles in the body, including:

* Regulating fluid balance: Sodium helps to regulate the amount of water in and around your cells, which is important for maintaining normal blood pressure and preventing dehydration.
* Facilitating nerve impulse transmission: Sodium is involved in the generation and transmission of electrical signals in the nervous system, which is necessary for proper muscle function and coordination.
* Assisting with muscle contraction: Sodium helps to regulate muscle contractions by interacting with other minerals such as calcium and potassium.

Low sodium levels (hyponatremia) can cause symptoms such as confusion, seizures, and coma, while high sodium levels (hypernatremia) can lead to symptoms such as weakness, muscle cramps, and seizures. Both conditions require medical treatment to correct.

Pseudohypoaldosteronism is a group of disorders that are characterized by resistance to aldosterone, a hormone produced by the adrenal glands. Aldosterone plays a key role in regulating sodium and potassium balance in the body. In pseudohypoaldosteronism, the kidneys fail to respond to aldosterone, leading to an imbalance of electrolytes in the body.

There are two types of pseudohypoaldosteronism: type I and type II. Type I is further divided into two subtypes: severe neonatal or infantile forms, which are usually caused by genetic mutations that affect the function of the sodium-potassium pump in the kidney; and milder forms, which can be inherited or acquired and may be associated with other medical conditions.

Type II pseudohypoaldosteronism is a rare disorder that typically affects older children and adults. It is caused by genetic mutations that affect the function of the mineralocorticoid receptor in the kidney, which binds to aldosterone and triggers a response.

Symptoms of pseudohypoaldosteronism may include low sodium levels, high potassium levels, and metabolic acidosis (a buildup of acid in the body). Treatment typically involves supplementation with sodium and/or medications to help regulate electrolyte balance.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Sodium chloride, commonly known as salt, is an essential electrolyte in dietary intake. It is a chemical compound made up of sodium (Na+) and chloride (Cl-) ions. In a medical context, particularly in nutrition and dietetics, "sodium chloride, dietary" refers to the consumption of this compound in food sources.

Sodium plays a crucial role in various bodily functions such as maintaining fluid balance, assisting nerve impulse transmission, and contributing to muscle contraction. The Dietary Guidelines for Americans recommend limiting sodium intake to less than 2,300 milligrams (mg) per day and further suggest an ideal limit of no more than 1,500 mg per day for most adults, especially those with high blood pressure. However, the average American consumes more than twice the recommended amount, primarily from processed and prepared foods. Excessive sodium intake can lead to high blood pressure and increase the risk of heart disease and stroke.

Cortisone is a type of corticosteroid hormone that is produced naturally in the body by the adrenal gland. It is released in response to stress and helps to regulate metabolism, reduce inflammation, and suppress the immune system. Cortisone can also be synthetically produced and is often used as a medication to treat a variety of conditions such as arthritis, asthma, and skin disorders. It works by mimicking the effects of the natural hormone in the body and reducing inflammation and suppressing the immune system. Cortisone can be administered through various routes, including oral, injectable, topical, and inhalational.

Tetrahydrocortisol (THF) is a metabolite of cortisol, which is a natural hormone produced by the adrenal gland in response to stress. Cortisol has various functions in the body, including regulating metabolism, immune response, and stress reaction.

Tetrahydrocortisol is formed when cortisol undergoes reduction in the liver by the enzyme 5β-reductase. It is a weak glucocorticoid with minimal biological activity compared to cortisol. Tetrahydrocortisol is primarily used as a biomarker for assessing cortisol production and metabolism in research and clinical settings, particularly in the diagnosis of disorders related to the adrenal gland or hypothalamic-pituitary-adrenal (HPA) axis.

There are two major types of tetrahydrocortisol: 5β-tetrahydrocortisol (5β-THF) and 5α-tetrahydrocortisol (5α-THF). The ratio of these two forms can provide additional information about cortisol metabolism, as the activity of 5β-reductase may vary in different individuals or under certain conditions.

Steroid 11-beta-hydroxylase is a crucial enzyme involved in the steroidogenesis pathway, specifically in the synthesis of cortisol and aldosterone, which are vital hormones produced by the adrenal glands. This enzyme is encoded by the CYP11B1 gene in humans.

The enzyme's primary function is to catalyze the conversion of 11-deoxycortisol to cortisol and 11-deoxycorticosterone to aldosterone through the process of hydroxylation at the 11-beta position of the steroid molecule. Cortisol is a critical glucocorticoid hormone that helps regulate metabolism, immune response, and stress response, while aldosterone is a mineralocorticoid hormone responsible for maintaining electrolyte and fluid balance in the body.

Deficiencies or mutations in the CYP11B1 gene can lead to various disorders, such as congenital adrenal hyperplasia (CAH), which may result in impaired cortisol and aldosterone production, causing hormonal imbalances and associated symptoms.

Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.

Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.

If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.

18-Hydroxycorticosterone is a steroid hormone that is produced in the adrenal gland. It is an intermediate in the biosynthesis of aldosterone, which is the major hormone responsible for regulating sodium and potassium balance in the body. 18-Hydroxycorticosterone gets its name from the hydroxyl group (-OH) that is added to the 18th carbon atom of the steroid molecule.

This hormone plays a role in the body's response to stress and helps to regulate various physiological processes, including metabolism, immune function, and sexual development and reproduction. However, abnormal levels of 18-hydroxycorticosterone have been associated with certain medical conditions, such as primary aldosteronism, which is a condition characterized by the overproduction of aldosterone.

It's important to note that while 18-hydroxycorticosterone is an important hormone in the body, it is not typically measured in routine clinical testing. Instead, tests for aldosterone and related hormones are more commonly used to diagnose and manage conditions related to the adrenal gland.

I am not aware of a medical definition for "Cortodoxone." It is possible that this term is not recognized in the field of medicine as it does not appear to be a commonly used medication, treatment, or diagnostic tool. If you have any more information about where you encountered this term or its potential meaning, I would be happy to try and provide further clarification.

11-Beta-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1) is an enzyme that plays a crucial role in the metabolism of steroid hormones, particularly cortisol, in the body. Cortisol is a glucocorticoid hormone produced by the adrenal glands that helps regulate various physiological processes such as metabolism, immune response, and stress response.

11β-HSD1 is primarily expressed in liver, fat, and muscle tissues, where it catalyzes the conversion of cortisone to cortisol. Cortisone is a biologically inactive form of cortisol that is produced when cortisol levels are high, and it needs to be converted back to cortisol for the hormone to exert its effects.

By increasing the availability of active cortisol in these tissues, 11β-HSD1 has been implicated in several metabolic disorders, including obesity, insulin resistance, and type 2 diabetes. Inhibitors of 11β-HSD1 are currently being investigated as potential therapeutic agents for the treatment of these conditions.

Renin is a medically recognized term and it is defined as:

"A protein (enzyme) that is produced and released by specialized cells (juxtaglomerular cells) in the kidney. Renin is a key component of the renin-angiotensin-aldosterone system (RAAS), which helps regulate blood pressure and fluid balance in the body.

When the kidney detects a decrease in blood pressure or a reduction in sodium levels, it releases renin into the bloodstream. Renin then acts on a protein called angiotensinogen, converting it to angiotensin I. Angiotensin-converting enzyme (ACE) subsequently converts angiotensin I to angiotensin II, which is a potent vasoconstrictor that narrows blood vessels and increases blood pressure.

Additionally, angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption in the kidneys and increases water retention, further raising blood pressure.

Therefore, renin plays a critical role in maintaining proper blood pressure and electrolyte balance in the body."

Steroid receptors are a type of nuclear receptor protein that are activated by the binding of steroid hormones or related molecules. These receptors play crucial roles in various physiological processes, including development, homeostasis, and metabolism. Steroid receptors function as transcription factors, regulating gene expression when activated by their respective ligands.

There are several subtypes of steroid receptors, classified based on the specific steroid hormones they bind to:

1. Glucocorticoid receptor (GR): Binds to glucocorticoids, which regulate metabolism, immune response, and stress response.
2. Mineralocorticoid receptor (MR): Binds to mineralocorticoids, which regulate electrolyte and fluid balance.
3. Androgen receptor (AR): Binds to androgens, which are male sex hormones that play a role in the development and maintenance of male sexual characteristics.
4. Estrogen receptor (ER): Binds to estrogens, which are female sex hormones that play a role in the development and maintenance of female sexual characteristics.
5. Progesterone receptor (PR): Binds to progesterone, which is a female sex hormone involved in the menstrual cycle and pregnancy.
6. Vitamin D receptor (VDR): Binds to vitamin D, which plays a role in calcium homeostasis and bone metabolism.

Upon ligand binding, steroid receptors undergo conformational changes that allow them to dimerize, interact with co-regulatory proteins, and bind to specific DNA sequences called hormone response elements (HREs) in the promoter regions of target genes. This interaction leads to the recruitment of transcriptional machinery, ultimately resulting in the modulation of gene expression. Dysregulation of steroid receptor signaling has been implicated in various diseases, including cancer, metabolic disorders, and inflammatory conditions.

The Renin-Angiotensin System (RAS) is a complex hormonal system that regulates blood pressure, fluid and electrolyte balance, and vascular resistance. It plays a crucial role in the pathophysiology of hypertension, heart failure, and kidney diseases.

Here's a brief overview of how it works:

1. Renin is an enzyme that is released by the juxtaglomerular cells in the kidneys in response to decreased blood pressure or reduced salt delivery to the distal tubules.
2. Renin acts on a protein called angiotensinogen, which is produced by the liver, converting it into angiotensin I.
3. Angiotensin-converting enzyme (ACE), found in the lungs and other tissues, then converts angiotensin I into angiotensin II, a potent vasoconstrictor that narrows blood vessels and increases blood pressure.
4. Angiotensin II also stimulates the release of aldosterone from the adrenal glands, which promotes sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.
5. Additionally, angiotensin II has direct effects on the heart, promoting hypertrophy and remodeling, which can contribute to heart failure.
6. The RAS can be modulated by various medications, such as ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists, which are commonly used to treat hypertension, heart failure, and kidney diseases.

Blood pressure is the force exerted by circulating blood on the walls of the blood vessels. It is measured in millimeters of mercury (mmHg) and is given as two figures:

1. Systolic pressure: This is the pressure when the heart pushes blood out into the arteries.
2. Diastolic pressure: This is the pressure when the heart rests between beats, allowing it to fill with blood.

Normal blood pressure for adults is typically around 120/80 mmHg, although this can vary slightly depending on age, sex, and other factors. High blood pressure (hypertension) is generally considered to be a reading of 130/80 mmHg or higher, while low blood pressure (hypotension) is usually defined as a reading below 90/60 mmHg. It's important to note that blood pressure can fluctuate throughout the day and may be affected by factors such as stress, physical activity, and medication use.

Tetrahydrocortisone is a physiological inactive end product of cortisol metabolism. It's a type of steroid hormone that is produced by the adrenal gland and plays a role in the response to stress, the regulation of metabolism, and the immune system.

Tetrahydrocortisone is formed when cortisol, also known as hydrocortisone, is metabolized in the liver by the enzyme 3α-hydroxysteroid dehydrogenase (3α-HSD). This reaction converts cortisol to tetrahydrocortisone, which is then conjugated with glucuronic acid and excreted in the urine.

Tetrahydrocortisone has no known biological activity, and its measurement in the body is primarily used as a marker for cortisol metabolism. Abnormal levels of tetrahydrocortisone may indicate disorders of cortisol metabolism or adrenal gland function.

Carbenoxolone is a synthetic derivative of glycyrrhizin, which is found in the root of the licorice plant. It has been used in the treatment of gastric and duodenal ulcers due to its ability to increase the mucosal resistance and promote healing. Carbenoxolone works by inhibiting the enzyme 11-beta-hydroxysteroid dehydrogenase, which leads to an increase in the levels of cortisol and other steroids in the body. This can have various effects on the body, including anti-inflammatory and immunosuppressive actions.

However, long-term use of carbenoxolone has been associated with serious side effects such as hypertension, hypokalemia (low potassium levels), and edema (fluid retention). Therefore, its use is generally limited to short-term treatment of gastric and duodenal ulcers.

Medical Definition: Carbenoxolone

A synthetic derivative of glycyrrhizin, used in the treatment of gastric and duodenal ulcers due to its ability to increase mucosal resistance and promote healing. It is an inhibitor of 11-beta-hydroxysteroid dehydrogenase, leading to increased levels of cortisol and other steroids in the body, with potential anti-inflammatory and immunosuppressive effects. However, long-term use is associated with serious side effects such as hypertension, hypokalemia, and edema.

Distal kidney tubules are the final segment of the renal tubule in the nephron of the kidney. The nephron is the basic unit of the kidney that filters blood and produces urine. After the filtrate leaves the glomerulus, it enters the proximal tubule where most of the reabsorption of water, electrolytes, and nutrients occurs.

The filtrate then moves into the loop of Henle, which is divided into a thin and thick descending limb and a thin and thick ascending limb. The loop of Henle helps to establish a concentration gradient in the medullary interstitium, allowing for the reabsorption of water in the collecting ducts.

The distal tubule is the last segment of the renal tubule before the filtrate enters the collecting duct. It is a relatively short structure that receives filtrate from the thick ascending limb of the loop of Henle. The distal tubule plays an important role in regulating electrolyte and water balance by actively transporting ions such as sodium, potassium, and chloride.

The distal tubule also contains specialized cells called principal cells and intercalated cells that are responsible for secreting or reabsorbing hydrogen and potassium ions to maintain acid-base balance. Additionally, the distal tubule is a site of action for several hormones, including aldosterone, which stimulates sodium reabsorption and potassium excretion, and vasopressin (antidiuretic hormone), which promotes water reabsorption in the collecting ducts.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Adrenocorticotropic Hormone (ACTH) is a hormone produced and released by the anterior pituitary gland, a small endocrine gland located at the base of the brain. ACTH plays a crucial role in the regulation of the body's stress response and has significant effects on various physiological processes.

The primary function of ACTH is to stimulate the adrenal glands, which are triangular-shaped glands situated on top of the kidneys. The adrenal glands consist of two parts: the outer cortex and the inner medulla. ACTH specifically targets the adrenal cortex, where it binds to specific receptors and initiates a series of biochemical reactions leading to the production and release of steroid hormones, primarily cortisol (a glucocorticoid) and aldosterone (a mineralocorticoid).

Cortisol is involved in various metabolic processes, such as regulating blood sugar levels, modulating the immune response, and helping the body respond to stress. Aldosterone plays a vital role in maintaining electrolyte and fluid balance by promoting sodium reabsorption and potassium excretion in the kidneys.

ACTH release is controlled by the hypothalamus, another part of the brain, which produces corticotropin-releasing hormone (CRH). CRH stimulates the anterior pituitary gland to secrete ACTH, which in turn triggers cortisol production in the adrenal glands. This complex feedback system helps maintain homeostasis and ensures that appropriate amounts of cortisol are released in response to various physiological and psychological stressors.

Disorders related to ACTH can lead to hormonal imbalances, resulting in conditions such as Cushing's syndrome (excessive cortisol production) or Addison's disease (insufficient cortisol production). Proper diagnosis and management of these disorders typically involve assessing the function of the hypothalamic-pituitary-adrenal axis and addressing any underlying issues affecting ACTH secretion.

Androstanols are a class of steroid compounds that contain a skeleton of 17 carbon atoms arranged in a particular structure. They are derived from androstane, which is a reduced form of testosterone, a male sex hormone. Androstanols have a variety of biological activities and can be found in various tissues and bodily fluids, including sweat, urine, and blood.

In the context of medical research and diagnostics, androstanols are sometimes used as biomarkers to study various physiological processes and diseases. For example, some studies have investigated the use of androstanol metabolites in urine as markers for prostate cancer. However, more research is needed to establish their clinical utility.

It's worth noting that while androstanols are related to steroid hormones, they do not have the same hormonal activity as testosterone or other sex hormones. Instead, they may play a role in cell signaling and other regulatory functions within the body.

Congenital Adrenal Hyperplasia (CAH) is a group of inherited genetic disorders that affect the adrenal glands, which are triangular-shaped glands located on top of the kidneys. The adrenal glands are responsible for producing several essential hormones, including cortisol, aldosterone, and androgens.

CAH is caused by mutations in genes that code for enzymes involved in the synthesis of these hormones. The most common form of CAH is 21-hydroxylase deficiency, which affects approximately 90% to 95% of all cases. Other less common forms of CAH include 11-beta-hydroxylase deficiency and 3-beta-hydroxysteroid dehydrogenase deficiency.

The severity of the disorder can vary widely, depending on the degree of enzyme deficiency. In severe cases, the lack of cortisol production can lead to life-threatening salt wasting and electrolyte imbalances in newborns. The excess androgens produced due to the enzyme deficiency can also cause virilization, or masculinization, of female fetuses, leading to ambiguous genitalia at birth.

In milder forms of CAH, symptoms may not appear until later in childhood or even adulthood. These may include early puberty, rapid growth followed by premature fusion of the growth plates and short stature, acne, excessive hair growth, irregular menstrual periods, and infertility.

Treatment for CAH typically involves replacing the missing hormones with medications such as hydrocortisone, fludrocortisone, and/or sex hormones. Regular monitoring of hormone levels and careful management of medication doses is essential to prevent complications such as adrenal crisis, growth suppression, and osteoporosis.

In severe cases of CAH, early diagnosis and treatment can help prevent or minimize the risk of serious health problems and improve quality of life. Genetic counseling may also be recommended for affected individuals and their families to discuss the risks of passing on the disorder to future generations.

Electrolytes are substances that, when dissolved in water, break down into ions that can conduct electricity. In the body, electrolytes are responsible for regulating various important physiological functions, including nerve and muscle function, maintaining proper hydration and acid-base balance, and helping to repair tissue damage.

The major electrolytes found in the human body include sodium, potassium, chloride, bicarbonate, calcium, magnesium, and phosphate. These electrolytes are tightly regulated by various mechanisms, including the kidneys, which help to maintain their proper balance in the body.

When there is an imbalance of electrolytes in the body, it can lead to a range of symptoms and health problems. For example, low levels of sodium (hyponatremia) can cause confusion, seizures, and even coma, while high levels of potassium (hyperkalemia) can lead to heart arrhythmias and muscle weakness.

Electrolytes are also lost through sweat during exercise or illness, so it's important to replace them through a healthy diet or by drinking fluids that contain electrolytes, such as sports drinks or coconut water. In some cases, electrolyte imbalances may require medical treatment, such as intravenous (IV) fluids or medication.

Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.

Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.

Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.

Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:

1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.

The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.

Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.

Hydroxyprogesterone is a synthetic form of the natural hormone progesterone, which is produced by the body during pregnancy to support the growth and development of the fetus. Hydroxyprogesterone is used in medical treatments to help prevent preterm birth in certain high-risk pregnancies.

There are several different forms of hydroxyprogesterone that have been developed for use as medications, including:

1. Hydroxyprogesterone caproate (HPC): This is a synthetic form of progesterone that is given as an injection once a week to help prevent preterm birth in women who have previously given birth prematurely. It works by helping to thicken the lining of the uterus and prevent contractions.
2. 17-Hydroxyprogesterone: This is a natural hormone that is produced by the body during pregnancy, but it can also be synthesized in a laboratory for use as a medication. It has been studied for its potential to help prevent preterm birth, although it is not currently approved for this use by the U.S. Food and Drug Administration (FDA).
3. 21-Hydroxyprogesterone: This is another natural hormone that is produced by the body during pregnancy, but it can also be synthesized in a laboratory for use as a medication. It has been studied for its potential to help prevent preterm birth and for its ability to reduce the risk of certain complications in women with a history of premature birth.

It's important to note that hydroxyprogesterone should only be used under the supervision of a healthcare provider, as it can have side effects and may not be appropriate for all women. If you are pregnant or planning to become pregnant and have concerns about preterm birth, it's important to discuss your options with your healthcare provider.

Oxyphenbutazone is a non-selective non-steroidal anti-inflammatory drug (NSAID) that has been used in the past for its analgesic, anti-inflammatory, and antipyretic properties. It works by inhibiting the enzyme cyclooxygenase (COX), which is involved in the synthesis of prostaglandins, chemicals that mediate inflammation, pain, and fever.

However, due to its potential for serious side effects such as gastrointestinal ulcers, bleeding, and kidney damage, as well as interactions with other medications, oxyphenbutazone is no longer commonly used in many countries. It has been largely replaced by newer NSAIDs that have a more favorable safety profile.

It's important to note that the use of oxyphenbutazone should be under the strict supervision of a healthcare professional and should only be taken as directed, as it can cause potentially serious side effects even at therapeutic doses.

The adrenal cortex hormones are a group of steroid hormones produced and released by the outer portion (cortex) of the adrenal glands, which are located on top of each kidney. These hormones play crucial roles in regulating various physiological processes, including:

1. Glucose metabolism: Cortisol helps control blood sugar levels by increasing glucose production in the liver and reducing its uptake in peripheral tissues.
2. Protein and fat metabolism: Cortisol promotes protein breakdown and fatty acid mobilization, providing essential building blocks for energy production during stressful situations.
3. Immune response regulation: Cortisol suppresses immune function to prevent overactivation and potential damage to the body during stress.
4. Cardiovascular function: Aldosterone regulates electrolyte balance and blood pressure by promoting sodium reabsorption and potassium excretion in the kidneys.
5. Sex hormone production: The adrenal cortex produces small amounts of sex hormones, such as androgens and estrogens, which contribute to sexual development and function.
6. Growth and development: Cortisol plays a role in normal growth and development by influencing the activity of growth-promoting hormones like insulin-like growth factor 1 (IGF-1).

The main adrenal cortex hormones include:

1. Glucocorticoids: Cortisol is the primary glucocorticoid, responsible for regulating metabolism and stress response.
2. Mineralocorticoids: Aldosterone is the primary mineralocorticoid, involved in electrolyte balance and blood pressure regulation.
3. Androgens: Dehydroepiandrosterone (DHEA) and its sulfate derivative (DHEAS) are the most abundant adrenal androgens, contributing to sexual development and function.
4. Estrogens: Small amounts of estrogens are produced by the adrenal cortex, mainly in women.

Disorders related to impaired adrenal cortex hormone production or regulation can lead to various clinical manifestations, such as Addison's disease (adrenal insufficiency), Cushing's syndrome (hypercortisolism), and congenital adrenal hyperplasia (CAH).

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Hydroxycorticosteroids are a class of corticosteroid hormones that contain a hydroxyl group at the 11-beta position. They include naturally occurring hormones such as cortisol and artificially produced drugs used to treat various conditions like inflammation, autoimmune diseases, and allergies. These medications work by mimicking the effects of hormones produced in the adrenal gland, reducing inflammation and suppressing the immune system. Examples of hydroxycorticosteroids include cortisone, prednisone, and dexamethasone.

The adrenal glands are a pair of endocrine glands that are located on top of the kidneys. Each gland has two parts: the outer cortex and the inner medulla. The adrenal cortex produces hormones such as cortisol, aldosterone, and androgens, which regulate metabolism, blood pressure, and other vital functions. The adrenal medulla produces catecholamines, including epinephrine (adrenaline) and norepinephrine (noradrenaline), which help the body respond to stress by increasing heart rate, blood pressure, and alertness.

Androstenediols are endogenous steroid hormones that are produced in the body from dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS), which are secreted by the adrenal glands. There are two major types of androstenediols: 5-androstenediol and 4-androstenediol. These hormones can be further metabolized into testosterone and estrogens, making them important intermediates in steroid hormone synthesis.

5-androstenediol is a weak androgen that can be converted to testosterone in peripheral tissues, while 4-androstenediol has little known biological activity. Both of these compounds have been studied for their potential role in various physiological processes, including sexual differentiation, bone metabolism, and aging. However, more research is needed to fully understand their functions and clinical significance.

It's worth noting that androstenediols are also sometimes referred to as "prohormones" because they can be converted into active steroid hormones in the body. Some athletes and bodybuilders have used synthetic forms of these compounds as performance-enhancing drugs, although their use is banned by many sports organizations due to concerns about potential health risks and unfair advantages in competition.

Sodium chloride symporters are membrane transport proteins that actively co-transport sodium and chloride ions into a cell. They are also known as sodium-chloride cotransporters or NCCs. These transporters play a crucial role in regulating the electrolyte balance and water homeostasis in various tissues, particularly in the kidney's distal convoluted tubule.

The primary function of sodium chloride symporters is to reabsorb sodium and chloride ions from the filtrate in the nephron back into the bloodstream. By doing so, they help maintain the body's sodium concentration and control water balance through osmosis.

Mutations in the gene encoding for the NCC can lead to various kidney disorders, such as Gitelman syndrome or Bartter syndrome type III, which are characterized by electrolyte imbalances, low blood pressure, and metabolic alkalosis.

Triamterene is a potassium-sparing diuretic (a type of "water pill") that is used to treat fluid retention (edema) and high blood pressure. It works by preventing your body from absorbing too much salt and keeps your potassium levels from getting too low.

The medical definition of Triamterene, according to the National Library of Medicine's MedlinePlus, is: "A medication that helps to reduce the amount of fluid in the body by increasing the amount of urine produced. It is used to treat high blood pressure and edema (fluid retention)."

Triamterene is available only with a prescription and is typically taken by mouth in the form of a tablet, usually two or three times a day after meals. Common side effects include headache, dizziness, and stomach upset. It is important to follow your healthcare provider's instructions carefully when taking this medication, as it can have serious interactions with other medications and may cause an imbalance of electrolytes in the body if not used properly.

Adrenocortical hyperfunction, also known as Cushing's syndrome, is a condition characterized by the overproduction of cortisol hormone from the adrenal glands. The adrenal glands are located on top of the kidneys and are responsible for producing several essential hormones, including cortisol. Cortisol helps regulate metabolism, blood pressure, and the body's response to stress.

In Adrenocortical hyperfunction, the adrenal glands produce too much cortisol, leading to a range of symptoms such as weight gain, particularly around the trunk and face, thinning of the skin, easy bruising, muscle weakness, mood changes, and high blood pressure. The condition can be caused by several factors, including tumors in the pituitary gland or adrenal glands, long-term use of corticosteroid medications, or genetic disorders that affect the adrenal glands.

Treatment for Adrenocortical hyperfunction depends on the underlying cause of the condition and may include surgery to remove tumors, medication to reduce cortisol production, or radiation therapy. It is essential to diagnose and treat this condition promptly, as long-term exposure to high levels of cortisol can lead to serious health complications such as diabetes, osteoporosis, and heart disease.

The Hypothalamo-Hypophyseal system, also known as the hypothalamic-pituitary system, is a crucial part of the endocrine system that regulates many bodily functions. It consists of two main components: the hypothalamus and the pituitary gland.

The hypothalamus is a region in the brain that receives information from various parts of the body and integrates them to regulate vital functions such as body temperature, hunger, thirst, sleep, and emotional behavior. It also produces and releases neurohormones that control the secretion of hormones from the pituitary gland.

The pituitary gland is a small gland located at the base of the brain, just below the hypothalamus. It consists of two parts: the anterior pituitary (also called adenohypophysis) and the posterior pituitary (also called neurohypophysis). The anterior pituitary produces and releases several hormones that regulate various bodily functions such as growth, metabolism, reproduction, and stress response. The posterior pituitary stores and releases hormones produced by the hypothalamus, including antidiuretic hormone (ADH) and oxytocin.

The hypothalamo-hypophyseal system works together to maintain homeostasis in the body by regulating various physiological processes through hormonal signaling. Dysfunction of this system can lead to several endocrine disorders, such as diabetes insipidus, pituitary tumors, and hypothalamic-pituitary axis disorders.

Dietary sodium is a mineral that is primarily found in table salt (sodium chloride) and many processed foods. It is an essential nutrient for human health, playing a crucial role in maintaining fluid balance, transmitting nerve impulses, and regulating muscle contractions. However, consuming too much dietary sodium can increase blood pressure and contribute to the development of hypertension, heart disease, stroke, and kidney problems.

The recommended daily intake of dietary sodium is less than 2,300 milligrams (mg) per day for most adults, but the American Heart Association recommends no more than 1,500 mg per day for optimal heart health. It's important to note that many processed and restaurant foods contain high levels of sodium, so it's essential to read food labels and choose fresh, whole foods whenever possible to help limit dietary sodium intake.

Sodium Chloride is defined as the inorganic compound with the chemical formula NaCl, representing a 1:1 ratio of sodium and chloride ions. It is commonly known as table salt or halite, and it is used extensively in food seasoning and preservation due to its ability to enhance flavor and inhibit bacterial growth. In medicine, sodium chloride is used as a balanced electrolyte solution for rehydration and as a topical wound irrigant and antiseptic. It is also an essential component of the human body's fluid balance and nerve impulse transmission.

Fibrosis is a pathological process characterized by the excessive accumulation and/or altered deposition of extracellular matrix components, particularly collagen, in various tissues and organs. This results in the formation of fibrous scar tissue that can impair organ function and structure. Fibrosis can occur as a result of chronic inflammation, tissue injury, or abnormal repair mechanisms, and it is a common feature of many diseases, including liver cirrhosis, lung fibrosis, heart failure, and kidney disease.

In medical terms, fibrosis is defined as:

"The process of producing scar tissue (consisting of collagen) in response to injury or chronic inflammation in normal connective tissue. This can lead to the thickening and stiffening of affected tissues and organs, impairing their function."

Steroid 21-hydroxylase, also known as CYP21A2, is a crucial enzyme involved in the synthesis of steroid hormones in the adrenal gland. Specifically, it catalyzes the conversion of 17-hydroxyprogesterone to 11-deoxycortisol and progesterone to deoxycorticosterone in the glucocorticoid and mineralocorticoid pathways, respectively.

Deficiency or mutations in this enzyme can lead to a group of genetic disorders called congenital adrenal hyperplasia (CAH), which is characterized by impaired cortisol production and disrupted hormonal balance. Depending on the severity of the deficiency, CAH can result in various symptoms such as ambiguous genitalia, precocious puberty, sexual infantilism, infertility, and increased risk of adrenal crisis.

The pituitary-adrenal system, also known as the hypothalamic-pituitary-adrenal (HPA) axis, is a complex set of interactions between the hypothalamus, the pituitary gland, and the adrenal glands. This system plays a crucial role in the body's response to stress through the release of hormones that regulate various physiological processes.

The hypothalamus, located within the brain, receives information from the nervous system about the internal and external environment and responds by releasing corticotropin-releasing hormone (CRH) and vasopressin. These hormones then travel to the anterior pituitary gland, where they stimulate the release of adrenocorticotropic hormone (ACTH).

ACTH is transported through the bloodstream to the adrenal glands, which are located on top of the kidneys. The adrenal glands consist of two parts: the outer cortex and the inner medulla. ACTH specifically targets the adrenal cortex, causing it to release cortisol and other glucocorticoids, as well as androgens such as dehydroepiandrosterone (DHEA).

Cortisol has numerous effects on metabolism, immune function, and cardiovascular regulation. It helps regulate blood sugar levels, suppresses the immune system, and aids in the breakdown of fats, proteins, and carbohydrates to provide energy during stressful situations. DHEA can be converted into male and female sex hormones (androgens and estrogens) in various tissues throughout the body.

The pituitary-adrenal system is tightly regulated through negative feedback mechanisms. High levels of cortisol, for example, inhibit the release of CRH and ACTH from the hypothalamus and pituitary gland, respectively, thereby limiting further cortisol production. Dysregulation of this system has been implicated in several medical conditions, including Cushing's syndrome (overproduction of cortisol) and Addison's disease (underproduction of cortisol).

Adrenal gland diseases refer to a group of medical conditions that affect the function or structure of the adrenal glands. The adrenal glands are small, triangular-shaped glands located on top of each kidney. They are responsible for producing several essential hormones, including cortisol, aldosterone, and adrenaline (epinephrine).

There are various types of adrenal gland diseases, some of which include:

1. Adrenal Insufficiency: A condition where the adrenal glands do not produce enough hormones, particularly cortisol and aldosterone. This can lead to symptoms such as fatigue, weight loss, low blood pressure, and skin hyperpigmentation.
2. Cushing's Syndrome: A condition characterized by an excess of cortisol in the body. It can be caused by a tumor in the pituitary gland or adrenal glands, or it can result from long-term use of steroid medications.
3. Adrenal Cancer: A rare type of cancer that affects the adrenal glands. Symptoms may include abdominal pain, weight loss, and high blood pressure.
4. Pheochromocytoma: A tumor that develops in the adrenal glands and causes an overproduction of adrenaline (epinephrine) and noradrenaline (norepinephrine). Symptoms may include high blood pressure, headaches, sweating, and anxiety.
5. Adrenal Hemorrhage: A condition where bleeding occurs in the adrenal glands, often as a result of severe trauma or infection. This can lead to adrenal insufficiency and other complications.
6. Congenital Adrenal Hyperplasia: An inherited disorder that affects the production of cortisol and other hormones in the adrenal glands. Symptoms may include ambiguous genitalia, precocious puberty, and short stature.

Treatment for adrenal gland diseases varies depending on the specific condition and its severity. Treatment options may include medication, surgery, or radiation therapy.

The kidney cortex is the outer region of the kidney where most of the functional units called nephrons are located. It plays a crucial role in filtering blood and regulating water, electrolyte, and acid-base balance in the body. The kidney cortex contains the glomeruli, proximal tubules, loop of Henle, and distal tubules, which work together to reabsorb necessary substances and excrete waste products into the urine.

"Glycyrrhiza" is the medical term for the licorice plant (Glycyrrhiza glabra), which belongs to the legume family. The root of this plant contains glycyrrhizin, a sweet-tasting compound that has been used in traditional medicine for various purposes such as treating coughs, stomach ulcers, and liver disorders. However, excessive consumption of glycyrrhizin can lead to serious side effects like high blood pressure, low potassium levels, and even heart problems. Therefore, it is important to use licorice products under the guidance of a healthcare professional.

Water-electrolyte balance refers to the regulation of water and electrolytes (sodium, potassium, chloride, bicarbonate) in the body to maintain homeostasis. This is crucial for various bodily functions such as nerve impulse transmission, muscle contraction, fluid balance, and pH regulation. The body maintains this balance through mechanisms that control water intake, excretion, and electrolyte concentration in various body fluids like blood and extracellular fluid. Disruptions in water-electrolyte balance can lead to dehydration or overhydration, and imbalances in electrolytes can cause conditions such as hyponatremia (low sodium levels) or hyperkalemia (high potassium levels).

Immediate-early proteins (IEPs) are a class of regulatory proteins that play a crucial role in the early stages of gene expression in viral infection and cellular stress responses. These proteins are synthesized rapidly, without the need for new protein synthesis, after the induction of immediate-early genes (IEGs).

In the context of viral infection, IEPs are often the first proteins produced by the virus upon entry into the host cell. They function as transcription factors that bind to specific DNA sequences and regulate the expression of early and late viral genes required for replication and packaging of the viral genome.

IEPs can also be involved in modulating host cell signaling pathways, altering cell cycle progression, and inducing apoptosis (programmed cell death). Dysregulation of IEPs has been implicated in various diseases, including cancer and neurological disorders.

It is important to note that the term "immediate-early proteins" is primarily used in the context of viral infection, while in other contexts such as cellular stress responses or oncogene activation, these proteins may be referred to by different names, such as "early response genes" or "transcription factors."

Amiloride is a medication that belongs to a class of drugs called potassium-sparing diuretics. It works by preventing the reabsorption of salt and water in the kidneys, which helps to increase urine output and decrease fluid buildup in the body. At the same time, amiloride also helps to preserve the level of potassium in the body, which is why it is known as a potassium-sparing diuretic.

Amiloride is commonly used to treat high blood pressure, heart failure, and edema (fluid buildup) in the body. It is available in tablet form and is typically taken once or twice a day, with or without food. Common side effects of amiloride include headache, dizziness, and stomach upset.

It's important to note that amiloride can interact with other medications, including some over-the-counter products, so it's essential to inform your healthcare provider of all the medications you are taking before starting amiloride therapy. Additionally, regular monitoring of blood pressure, kidney function, and electrolyte levels is necessary while taking this medication.

Steroids, also known as corticosteroids, are a type of hormone that the adrenal gland produces in your body. They have many functions, such as controlling the balance of salt and water in your body and helping to reduce inflammation. Steroids can also be synthetically produced and used as medications to treat a variety of conditions, including allergies, asthma, skin conditions, and autoimmune disorders.

Steroid medications are available in various forms, such as oral pills, injections, creams, and inhalers. They work by mimicking the effects of natural hormones produced by your body, reducing inflammation and suppressing the immune system's response to prevent or reduce symptoms. However, long-term use of steroids can have significant side effects, including weight gain, high blood pressure, osteoporosis, and increased risk of infections.

It is important to note that anabolic steroids are a different class of drugs that are sometimes abused for their muscle-building properties. These steroids are synthetic versions of the male hormone testosterone and can have serious health consequences when taken in large doses or without medical supervision.

Sodium-Potassium-Exchanging ATPase (also known as Na+/K+ ATPase) is a type of active transporter found in the cell membrane of many types of cells. It plays a crucial role in maintaining the electrochemical gradient and membrane potential of animal cells by pumping sodium ions (Na+) out of the cell and potassium ions (K+) into the cell, using energy derived from ATP hydrolysis.

This transporter is composed of two main subunits: a catalytic α-subunit that contains the binding sites for Na+, K+, and ATP, and a regulatory β-subunit that helps in the proper targeting and functioning of the pump. The Na+/K+ ATPase plays a critical role in various physiological processes, including nerve impulse transmission, muscle contraction, and kidney function.

In summary, Sodium-Potassium-Exchanging ATPase is an essential membrane protein that uses energy from ATP to transport sodium and potassium ions across the cell membrane, thereby maintaining ionic gradients and membrane potentials necessary for normal cellular function.

A sodium-restricted diet is a meal plan designed to limit the amount of sodium (salt) intake. The recommended daily sodium intake for adults is less than 2,300 milligrams (mg), but for those with certain medical conditions such as high blood pressure, heart failure, or chronic kidney disease, a lower daily sodium limit of 1,500 to 2,000 mg may be recommended.

A sodium-restricted diet typically involves avoiding processed and packaged foods, which are often high in sodium, and limiting the use of salt when cooking or at the table. Fresh fruits, vegetables, lean proteins, and whole grains are encouraged as they are naturally low in sodium. It is important to read food labels carefully, as some foods may contain hidden sources of sodium.

Adhering to a sodium-restricted diet can help manage blood pressure, reduce fluid retention, and decrease the risk of heart disease and stroke. However, it is important to consult with a healthcare provider or a registered dietitian before starting any new diet plan to ensure that it meets individual nutritional needs and medical conditions.

Glycyrrhetinic acid is defined medically as a pentacyclic triterpenoid derived from glycyrrhizin, which is found in the root of licorice plants. It has been used in traditional medicine for its anti-inflammatory and expectorant properties.

Glycyrrhetinic acid works by inhibiting the enzyme 11-beta-hydroxysteroid dehydrogenase, which is responsible for converting cortisol to cortisone. This can lead to increased levels of cortisol in the body, which can have various effects, including lowering potassium levels and increasing sodium levels, leading to fluid retention and high blood pressure in some individuals.

In addition to its use in traditional medicine, glycyrrhetinic acid has been studied for its potential benefits in treating a variety of conditions, including cancer, HIV, and hepatitis. However, more research is needed to confirm these potential benefits and to fully understand the risks and side effects associated with its use.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Angiotensin II is a potent vasoactive peptide hormone that plays a critical role in the renin-angiotensin-aldosterone system (RAAS), which is a crucial regulator of blood pressure and fluid balance in the body. It is formed from angiotensin I through the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II has several physiological effects on various organs, including:

1. Vasoconstriction: Angiotensin II causes contraction of vascular smooth muscle, leading to an increase in peripheral vascular resistance and blood pressure.
2. Aldosterone release: Angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption and potassium excretion in the kidneys, thereby increasing water retention and blood volume.
3. Sympathetic nervous system activation: Angiotensin II activates the sympathetic nervous system, leading to increased heart rate and contractility, further contributing to an increase in blood pressure.
4. Thirst regulation: Angiotensin II stimulates the hypothalamus to increase thirst, promoting water intake and helping to maintain intravascular volume.
5. Cell growth and fibrosis: Angiotensin II has been implicated in various pathological processes, such as cell growth, proliferation, and fibrosis, which can contribute to the development of cardiovascular and renal diseases.

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are two classes of medications commonly used in clinical practice to target the RAAS by blocking the formation or action of angiotensin II, respectively. These drugs have been shown to be effective in managing hypertension, heart failure, and chronic kidney disease.

Kidney tubules are the structural and functional units of the kidney responsible for reabsorption, secretion, and excretion of various substances. They are part of the nephron, which is the basic unit of the kidney's filtration and reabsorption process.

There are three main types of kidney tubules:

1. Proximal tubule: This is the initial segment of the kidney tubule that receives the filtrate from the glomerulus. It is responsible for reabsorbing approximately 65% of the filtrate, including water, glucose, amino acids, and electrolytes.
2. Loop of Henle: This U-shaped segment of the tubule consists of a thin descending limb, a thin ascending limb, and a thick ascending limb. The loop of Henle helps to concentrate urine by creating an osmotic gradient that allows water to be reabsorbed in the collecting ducts.
3. Distal tubule: This is the final segment of the kidney tubule before it empties into the collecting duct. It is responsible for fine-tuning the concentration of electrolytes and pH balance in the urine by selectively reabsorbing or secreting substances such as sodium, potassium, chloride, and hydrogen ions.

Overall, kidney tubules play a critical role in maintaining fluid and electrolyte balance, regulating acid-base balance, and removing waste products from the body.

Methylprednisolone Hemisuccinate is a synthetic glucocorticoid drug, which is a salt of Methylprednisolone with hemisuccinic acid. It is often used in the treatment of various inflammatory and autoimmune conditions due to its potent anti-inflammatory and immunosuppressive effects.

Methylprednisolone Hemisuccinate is rapidly absorbed after intravenous or intramuscular administration, with a bioavailability of nearly 100%. It has a high penetration rate into body tissues, including the central nervous system, making it useful in the treatment of conditions such as multiple sclerosis and other inflammatory diseases of the brain and spinal cord.

Like other glucocorticoids, Methylprednisolone Hemisuccinate works by binding to specific receptors in cells, which leads to a decrease in the production of pro-inflammatory cytokines and an increase in the production of anti-inflammatory mediators. This results in a reduction in inflammation, swelling, and pain, as well as a suppression of the immune system's response to various stimuli.

Methylprednisolone Hemisuccinate is available under several brand names, including Solu-Medrol and Depo-Medrol. It is typically administered in hospital settings for the treatment of severe inflammatory conditions or as part of a treatment regimen for certain autoimmune diseases. As with all medications, it should be used under the close supervision of a healthcare provider, and its benefits and risks should be carefully weighed before use.

'Rats, Inbred Dahl' are a strain of laboratory rats that have been selectively bred for research purposes. They were first developed by Dr. Lewis L. Dahl in the 1960s at the University of Colorado School of Medicine. These rats are known for their susceptibility to develop high blood pressure (hypertension) and related cardiovascular diseases, making them a valuable model for studying hypertension and its complications.

Inbred Dahl rats are typically divided into two main strains: the Dahl Salt-Sensitive (SS/JrHsdMcwi or SS) rat and the Dahl Salt-Resistant (SR/JrHsdMcwi or SR) rat. When fed a high-salt diet, the SS rats develop severe hypertension, kidney damage, and cardiac hypertrophy, while the SR rats are relatively resistant to these effects.

The Inbred Dahl rats have contributed significantly to our understanding of the genetic and environmental factors that contribute to the development of hypertension and related disorders. They continue to be widely used in biomedical research today.

Hyperkalemia is a medical condition characterized by an elevated level of potassium (K+) in the blood serum, specifically when the concentration exceeds 5.0-5.5 mEq/L (milliequivalents per liter). Potassium is a crucial intracellular ion that plays a significant role in various physiological processes, including nerve impulse transmission, muscle contraction, and heart rhythm regulation.

Mild to moderate hyperkalemia might not cause noticeable symptoms but can still have harmful effects on the body, particularly on the cardiovascular system. Severe cases of hyperkalemia (potassium levels > 6.5 mEq/L) can lead to potentially life-threatening arrhythmias and heart failure.

Hyperkalemia may result from various factors, such as kidney dysfunction, hormonal imbalances, medication side effects, trauma, or excessive potassium intake. Prompt identification and management of hyperkalemia are essential to prevent severe complications and ensure proper treatment.

The kidney medulla is the inner portion of the renal pyramids in the kidney, consisting of multiple conical structures found within the kidney. It is composed of loops of Henle and collecting ducts responsible for concentrating urine by reabsorbing water and producing a hyperosmotic environment. The kidney medulla has a unique blood supply and is divided into an inner and outer zone, with the inner zone having a higher osmolarity than the outer zone. This region of the kidney helps regulate electrolyte and fluid balance in the body.

Fadrozole is a non-steroidal aromatase inhibitor drug that is used in the treatment of breast cancer. Aromatase inhibitors work by blocking the production of estrogen, which some types of breast cancer cells need to grow. By reducing the amount of estrogen in the body, fadrozole can help slow or stop the growth of these cancer cells.

Fadrozole is typically used as a treatment for postmenopausal women with hormone receptor-positive breast cancer. It may be used as a first-line therapy or after other treatments have failed. The drug is administered orally, and the typical dosage is 1-2 mg per day.

Like all medications, fadrozole can cause side effects, including hot flashes, nausea, vomiting, and joint pain. In some cases, it may also cause more serious side effects such as liver damage or an increased risk of bone fractures. Patients taking fadrozole should be monitored closely by their healthcare provider to ensure that the drug is working effectively and to manage any side effects that may occur.

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.

Batrachoidiformes is an order of primarily marine ray-finned fish that includes the genera Batrachoides, Halophryne, Porichthys, and Thalassophryne. These fish are characterized by having a stout body, large head, and strong, bony mouthparts. They are often called "toadfish" due to their warty skin and toad-like appearance. Some species have the ability to produce sounds, which they use for communication and mating. They are found in tropical and subtropical waters of the Atlantic and Pacific Oceans, as well as in the Mediterranean Sea.

Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) is a laboratory technique used in molecular biology to amplify and detect specific DNA sequences. This technique is particularly useful for the detection and quantification of RNA viruses, as well as for the analysis of gene expression.

The process involves two main steps: reverse transcription and polymerase chain reaction (PCR). In the first step, reverse transcriptase enzyme is used to convert RNA into complementary DNA (cDNA) by reading the template provided by the RNA molecule. This cDNA then serves as a template for the PCR amplification step.

In the second step, the PCR reaction uses two primers that flank the target DNA sequence and a thermostable polymerase enzyme to repeatedly copy the targeted cDNA sequence. The reaction mixture is heated and cooled in cycles, allowing the primers to anneal to the template, and the polymerase to extend the new strand. This results in exponential amplification of the target DNA sequence, making it possible to detect even small amounts of RNA or cDNA.

RT-PCR is a sensitive and specific technique that has many applications in medical research and diagnostics, including the detection of viruses such as HIV, hepatitis C virus, and SARS-CoV-2 (the virus that causes COVID-19). It can also be used to study gene expression, identify genetic mutations, and diagnose genetic disorders.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Sodium channels are specialized protein structures that are embedded in the membranes of excitable cells, such as nerve and muscle cells. They play a crucial role in the generation and transmission of electrical signals in these cells. Sodium channels are responsible for the rapid influx of sodium ions into the cell during the initial phase of an action potential, which is the electrical signal that travels along the membrane of a neuron or muscle fiber. This sudden influx of sodium ions causes the membrane potential to rapidly reverse, leading to the depolarization of the cell. After the action potential, the sodium channels close and become inactivated, preventing further entry of sodium ions and helping to restore the resting membrane potential.

Sodium channels are composed of a large alpha subunit and one or two smaller beta subunits. The alpha subunit forms the ion-conducting pore, while the beta subunits play a role in modulating the function and stability of the channel. Mutations in sodium channel genes have been associated with various inherited diseases, including certain forms of epilepsy, cardiac arrhythmias, and muscle disorders.

A melanocortin type 2 receptor (MC2R) is a G protein-coupled receptor that binds melanocortin peptides such as adrenocorticotropic hormone (ACTH). It is primarily expressed in the adrenal gland, specifically in the zona fasciculata of the cortex. Upon activation by ACTH, MC2R stimulates the production and release of steroid hormones, particularly cortisol, through the cAMP signaling pathway. Dysfunction in this receptor can lead to various endocrine disorders such as congenital adrenal hyperplasia and Cushing's disease.

Alkalosis is a medical condition that refers to an excess of bases or a decrease in the concentration of hydrogen ions (H+) in the blood, leading to a higher than normal pH level. The normal range for blood pH is typically between 7.35 and 7.45. A pH above 7.45 indicates alkalosis.

Alkalosis can be caused by several factors, including:

1. Metabolic alkalosis: This type of alkalosis occurs due to an excess of bicarbonate (HCO3-) in the body, which can result from conditions such as excessive vomiting, hyperventilation, or the use of certain medications like diuretics.
2. Respiratory alkalosis: This form of alkalosis is caused by a decrease in carbon dioxide (CO2) levels in the blood due to hyperventilation or other conditions that affect breathing, such as high altitude, anxiety, or lung disease.

Symptoms of alkalosis can vary depending on its severity and underlying cause. Mild alkalosis may not produce any noticeable symptoms, while severe cases can lead to muscle twitching, cramps, tremors, confusion, and even seizures. Treatment for alkalosis typically involves addressing the underlying cause and restoring the body's normal pH balance through medications or other interventions as necessary.

Cardiac myocytes are the muscle cells that make up the heart muscle, also known as the myocardium. These specialized cells are responsible for contracting and relaxing in a coordinated manner to pump blood throughout the body. They differ from skeletal muscle cells in several ways, including their ability to generate their own electrical impulses, which allows the heart to function as an independent rhythmical pump. Cardiac myocytes contain sarcomeres, the contractile units of the muscle, and are connected to each other by intercalated discs that help coordinate contraction and ensure the synchronous beating of the heart.

The adrenal cortex is the outer portion of the adrenal gland, which is located on top of the kidneys. It plays a crucial role in producing hormones that are essential for various bodily functions. The adrenal cortex is divided into three zones:

1. Zona glomerulosa: This outermost zone produces mineralocorticoids, primarily aldosterone. Aldosterone helps regulate sodium and potassium balance and thus influences blood pressure by controlling the amount of fluid in the body.
2. Zona fasciculata: The middle layer is responsible for producing glucocorticoids, with cortisol being the most important one. Cortisol regulates metabolism, helps manage stress responses, and has anti-inflammatory properties. It also plays a role in blood sugar regulation and maintaining the body's response to injury and illness.
3. Zona reticularis: The innermost zone produces androgens, primarily dehydroepiandrosterone (DHEA) and its sulfate form (DHEAS). These androgens are weak compared to those produced by the gonads (ovaries or testes), but they can be converted into more potent androgens or estrogens in peripheral tissues.

Disorders related to the adrenal cortex can lead to hormonal imbalances, affecting various bodily functions. Examples include Addison's disease (insufficient adrenal cortical hormone production) and Cushing's syndrome (excessive glucocorticoid levels).

Sodium radioisotopes are unstable forms of sodium, an element naturally occurring in the human body, that emit radiation as they decay over time. These isotopes can be used for medical purposes such as imaging and treatment of various diseases. Commonly used sodium radioisotopes include Sodium-22 (^22Na) and Sodium-24 (^24Na).

It's important to note that the use of radioisotopes in medicine should be under the supervision of trained medical professionals, as improper handling or exposure can pose health risks.

Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.

The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.

Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.

The term "drinking" is commonly used to refer to the consumption of beverages, but in a medical context, it usually refers to the consumption of alcoholic drinks. According to the Merriam-Webster Medical Dictionary, "drinking" is defined as:

1. The act or habit of swallowing liquid (such as water, juice, or alcohol)
2. The ingestion of alcoholic beverages

It's important to note that while moderate drinking may not pose significant health risks for some individuals, excessive or binge drinking can lead to a range of negative health consequences, including addiction, liver disease, heart disease, and increased risk of injury or violence.

Diuretics are a type of medication that increase the production of urine and help the body eliminate excess fluid and salt. They work by interfering with the reabsorption of sodium in the kidney tubules, which in turn causes more water to be excreted from the body. Diuretics are commonly used to treat conditions such as high blood pressure, heart failure, liver cirrhosis, and kidney disease. There are several types of diuretics, including loop diuretics, thiazide diuretics, potassium-sparing diuretics, and osmotic diuretics, each with its own mechanism of action and potential side effects. It is important to use diuretics under the guidance of a healthcare professional, as they can interact with other medications and have an impact on electrolyte balance in the body.

Buthionine Sulfoximine (BSO) is a chemical compound that is known to inhibit the enzyme gamma-glutamylcysteine synthetase, which plays a crucial role in the production of glutathione, a powerful antioxidant in the body. By inhibiting this enzyme, BSO can deplete glutathione levels in cells, making it a useful tool in research to study the effects of glutathione depletion on various biological processes. It is often used in laboratory experiments and clinical trials for its potential therapeutic benefits in cancer treatment and other diseases associated with oxidative stress. However, its use as a therapeutic agent is still being investigated and has not yet been approved by regulatory agencies for widespread clinical use.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Metyrapone is a medication that is primarily used in the diagnosis and treatment of Cushing's syndrome, a condition characterized by excessive levels of cortisol hormone in the body. It works as an inhibitor of steroidogenesis, specifically blocking the enzyme 11-beta-hydroxylase, which is involved in the production of cortisol in the adrenal gland.

By inhibiting this enzyme, metyrapone prevents the formation of cortisol and leads to an accumulation of its precursor, 11-deoxycortisol. This can help restore the balance of hormones in the body and alleviate symptoms associated with Cushing's syndrome.

It is important to note that metyrapone should only be used under the supervision of a healthcare professional, as it can have significant side effects and interactions with other medications.

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The selective response of some tissues and organs to mineralocorticoids over glucocorticoids occurs because mineralocorticoid- ... "Human mineralocorticoid receptor interacts with actin under mineralocorticoid ligand modulation". FEBS Letters. 384 (2): 112-6 ... The mineralocorticoid receptor (or MR, MLR, MCR), also known as the aldosterone receptor or nuclear receptor subfamily 3, group ... Activation of the mineralocorticoid receptor, upon the binding of its ligand aldosterone, results in its translocation to the ...
... s (mMRs) or membrane aldosterone receptors are a group of receptors which bind and are ... Joëls M, Karst H, DeRijk R, de Kloet ER (2008). "The coming out of the brain mineralocorticoid receptor". Trends Neurosci. 31 ( ... Groeneweg FL, Karst H, de Kloet ER, Joëls M (2012). "Mineralocorticoid and glucocorticoid receptors at the neuronal membrane, ... Unlike the classical nuclear mineralocorticoid receptor (MR), which mediates its effects via genomic mechanisms, mMRs are cell ...
Apparent mineralocorticoid excess is a rare form of monogenic hypertension that is transmitted as an autosomal recessive trait ... Apparent mineralocorticoid excess at NIH's Office of Rare Diseases (CS1 Dutch-language sources (nl), CS1 maint: multiple names ... Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor due to the non-selectivity of the ... Apparent mineralocorticoid excess is an autosomal recessive disorder causing hypertension (high blood pressure), hypernatremia ...
Mineralocorticoids control the amount of potassium, sodium, and water in the body. Hypoadrenocorticism is fatal if left ... The zona glomerulosa is not controlled by ACTH, and remains able to produce a normal amount of mineralocorticoids. A dog with ... "Mineralocorticoids". School of Veterinary Medicine-Colorado State University. Retrieved 26 January 2011. Stoeppler, Melissa ... The adrenal glands secrete glucocorticoids such as cortisol and mineralocorticoids such as aldosterone; when proper amounts of ...
Gupta V (October 2011). "Mineralocorticoid hypertension". Indian Journal of Endocrinology and Metabolism. 15 Suppl 4 (8): S298- ... "Role of steroid 11 beta-hydroxylase and steroid 18-hydroxylase in the biosynthesis of glucocorticoids and mineralocorticoids in ...
"Serum steroid levels can help differentiate adrenal disorders". Gupta V (October 2011). "Mineralocorticoid hypertension". ... with mineralocorticoid activity. 11-deoxycortisol also takes part, by binding to specific corticosteroid receptors, in ... in which patients have low blood pressure from a lack of mineralocorticoids[original research?][dubious - discuss]). In 11β- ... and excess of 11-deoxycorticosterone leads to mineralocorticoid-based hypertension (as opposed to 21-hydroxylase deficiency, ...
Gupta V (October 2011). "Mineralocorticoid hypertension". Indian Journal of Endocrinology and Metabolism. 15 Suppl 4 (8): S298- ...
Slight SH, Joseph J, Ganjam VK, Weber KT (June 1999). "Extra-adrenal mineralocorticoids and cardiovascular tissue". Journal of ... Deactivation of enzymatic activity reduces aldosterone concentrations in plasma and tissues which decreases mineralocorticoid ... is a steroid hydroxylase cytochrome P450 enzyme involved in the biosynthesis of the mineralocorticoid aldosterone and other ... "Role of steroid 11 beta-hydroxylase and steroid 18-hydroxylase in the biosynthesis of glucocorticoids and mineralocorticoids in ...
Both drospirenone and progesterone are actually weak partial agonists of the MR in the absence of mineralocorticoids. Due to ... Drospirenone is an antagonist of the MR, the biological target of mineralocorticoids like aldosterone, and hence is an ... Infante M, Armani A, Marzolla V, Fabbri A, Caprio M (2019). "Adipocyte Mineralocorticoid Receptor". Vitamins and Hormones. ... and mineralocorticoid receptor (MR), with lower affinity to the androgen receptor (AR), and with very low affinity to the ...
Kolkhof P, Bärfacker L (2017). "30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor antagonists: 60 years of ... Maron BA, Leopold JA (2008). "Mineralocorticoid receptor antagonists and endothelial function". Curr Opin Investig Drugs. 9 (9 ... Sica DA (2005). "Pharmacokinetics and pharmacodynamics of mineralocorticoid blocking agents and their effects on potassium ... Parthasarathy HK, MacDonald TM (2007). "Mineralocorticoid receptor antagonists". Curr. Hypertens. Rep. 9 (1): 45-52. doi: ...
Kolkhof P, Bärfacker L (2017). "30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor antagonists: 60 years of ... Maron BA, Leopold JA (2008). "Mineralocorticoid receptor antagonists and endothelial function". Curr Opin Investig Drugs. 9 (9 ... Sica DA (2005). "Pharmacokinetics and pharmacodynamics of mineralocorticoid blocking agents and their effects on potassium ... Yang J, Young MJ (2016). "Mineralocorticoid receptor antagonists-pharmacodynamics and pharmacokinetic differences". Curr Opin ...
Kolkhof P, Bärfacker L (2017). "30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor antagonists: 60 years of ... Maron BA, Leopold JA (2008). "Mineralocorticoid receptor antagonists and endothelial function". Curr Opin Investig Drugs. 9 (9 ... Sica DA (2005). "Pharmacokinetics and pharmacodynamics of mineralocorticoid blocking agents and their effects on potassium ... Parthasarathy HK, MacDonald TM (2007). "Mineralocorticoid receptor antagonists". Curr. Hypertens. Rep. 9 (1): 45-52. doi: ...
... glycyrrhizin allows cortisol to activate mineralocorticoid receptors in the kidney. This severely potentiates mineralocorticoid ... Sabbadin C, Armanini D (September 2016). "Syndromes that mimic an excess of mineralocorticoids". High Blood Press Cardiovasc ... This cause of mineralocorticoid excess is primary hyperaldosteronism reflecting excess production of aldosterone by adrenal ...
In tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, it protects cells from the ... HSD-11β Type 2 is expressed by aldosterone-selective tissues and protects the mineralocorticoid receptor from the activation by ... Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension. The since the main functions ... To prevent over-stimulation of the mineralocorticoid receptor by cortisol, HSD-11βs convert the biologically active cortisol to ...
... impairs glucocorticoid and mineralocorticoid metabolism; causes glucocorticoid deficiency and mineralocorticoid excess as well ... impairs mineralocorticoid metabolism; results in mineralocorticoid excess In addition, several conditions of abnormal ... results in excessive mineralocorticoid activity 18-Hydroxylase deficiency: prevents mineralocorticoid synthesis; results in ... 21-Hydroxylase deficiency: prevents glucocorticoid and mineralocorticoid synthesis; causes androgen excess in females 11β- ...
Funder JW, Krozowski Z, Myles K, Sato A, Sheppard KE, Young M (1997). "Mineralocorticoid receptors, salt, and hypertension". ... glucocorticoids and mineralocorticoids (both corticosteroids) and androgens, estrogens, and progestogens (sex steroids). ... cortisone Mineralocorticoid: fludrocortisone Vitamin D: dihydrotachysterol Androgens: oxandrolone, oxabolone, nandrolone (also ...
It is a potent mineralocorticoid. Syntheses of 11β-OHP from progesterone is catalyzed by the steroid 11β-hydroxylase (CYP11B1) ... confer marked mineralocorticoid activity on corticosterone in the ADX rat". Endocrinology. 136 (4): 1809-12. doi:10.1210/endo. ... levels in late-onset adrenal 21-hydroxylase deficiency suggest a mild defect of the mineralocorticoid pathway". primary. The ...
... the neurobiology of the mineralocorticoid receptor; and impact of social deprivation on the incidence and management of ...
Hypertension and mineralocorticoid excess is treated with glucocorticoid replacement, as in other forms of CAH. Most genetic ... These features of mineralocorticoid excess are the major clinical clue distinguishing the more complete 17α-hydroxylase ... Thus, there is no mineralocorticoid overproduction. Also, there is no adrenal hyperplasia. It has also been observed in ... It causes decreased synthesis of cortisol and sex steroids, with resulting increase in mineralocorticoid production. Thus, ...
... acts as a highly selective antagonist of the mineralocorticoid receptor (Ki < 50 nM), the receptor for aldosterone ... Kolkhof P, Nowack C, Eitner F (2015). "Nonsteroidal antagonists of the mineralocorticoid receptor". Curr. Opin. Nephrol. ... Esaxerenone Finerenone "Apararenone - Mitsubishi Tanabe Pharma - AdisInsight". Yang J, Young MJ (2016). "Mineralocorticoid ...
ISBN 978-1-4051-4370-7. Maron BA, Leopold JA (September 2008). "Mineralocorticoid receptor antagonists and endothelial function ...
It also serves as a secondary stimulus for the synthesis of mineralocorticoids such as aldosterone, which serve an important ... "Syndromes of glucocorticoid and mineralocorticoid resistance". Steroids. 60 (1): 173-9. doi:10.1016/0039-128x(94)00007-y. PMID ...
It has very little mineralocorticoid effects. The affinities of triamcinolone acetonide for the androgen and estrogen receptors ...
Mineralocorticoids such as aldosterone are primarily involved in the regulation of electrolyte and water balance by modulating ... Typical mineralocorticoid side-effects are hypertension (abnormally high blood pressure), steroid induced diabetes mellitus, ... Corticosteroids act as agonists of the glucocorticoid receptor and/or the mineralocorticoid receptor. In addition to their ... Two main classes of corticosteroids, glucocorticoids and mineralocorticoids, are involved in a wide range of physiological ...
It acts as a highly selective silent antagonist of the mineralocorticoid receptor (MR), the receptor for aldosterone, with ... Kolkhof P, Nowack C, Eitner F (2015). "Nonsteroidal antagonists of the mineralocorticoid receptor". Curr. Opin. Nephrol. ... Apararenone Finerenone "Esaxerenone - Daiichi Sankyo - AdisInsight". Yang J, Young MJ (2016). "Mineralocorticoid receptor ...
The pharmacology and classification of the nuclear receptor superfamily: glucocorticoid, mineralocorticoid, progesterone, and ... Mineralocorticoid receptor (MR; NR3C2) (Aldosterone) 3: Progesterone receptor (PR; NR3C3, PGR) (Sex hormones: Progesterone) 4: ...
... mineralocorticoids and DHEA. In the short term, CRH can suppress appetite, increase subjective feelings of anxiety, and perform ...
... along with 10-fold reduced mineralocorticoid activity. In addition to its mineralocorticoid activity, DOC has been found to ... It is an active (Na+-retaining) mineralocorticoid. As its names indicate, 11-deoxycorticosterone can be understood as the 21- ... DOC is a potent mineralocorticoid but is virtually devoid of glucocorticoid activity. However, 11β-hydroxylation of DOC ... Pospísilová J, Pospísil M (1970). "Influence of mineralocorticoids on collagen synthesis in subcutaneous granuloma in ...
In these cases, mineralocorticoid deficiency emerges up to several years after birth. Sex steroid production may be sufficient ... Lipoid CAH causes mineralocorticoid deficiency in affected infants and children. Male infants are severely undervirilized ... In some cases, the condition is more mild with signs and symptoms of mineralocorticoid and glucocorticoid deficiency appearing ... Thus, there are no problems due to excessive mineralocorticoids or androgens. Third, lipid accumulation damages the testes and ...
Mineralocorticoids bind to the mineralocorticoid receptor in the cell cytosol, and are able to freely cross the lipid bilayer ... Mineralocorticoids are a class of corticosteroids, which in turn are a class of steroid hormones. Mineralocorticoids are ... 2008) Structure-function relationships in the mineralocorticoid receptor. J Mol Endocrinol. 41(6):405-13. Mineralocorticoids at ... The primary mineralocorticoid is aldosterone. The name mineralocorticoid derives from early observations that these hormones ...
Mineralocorticoid deficiency. Synonyms (terms occurring on more labels are shown first): mineralocorticoid deficiency More ...
Based on a wealth of validating preclinical studies, we contend that the favorable metabolic effects of mineralocorticoid ... Keywords: metabolic, mineralocorticoid receptor, diabetes, Calcineurin, Mineralocorticoid Receptor Antagonists, Transplantation ... Based on a wealth of validating preclinical studies, we contend that the favorable metabolic effects of mineralocorticoid ... Anti-Diabetogenic Properties of Mineralocorticoid Receptor Antagonists: Implications for Enhanced Safety and Efficacy of Post- ...
The physiological mineralocorticoid in ray-finned fish, which do not synthesize aldosterone, is not fully understood because ... Skate MR has a strong response to corticosteroids that are mineralocorticoids and glucocorticoids in humans. The half-maximal ... The mineralocorticoid receptor (MR) is descended from a corticoid receptor (CR), which has descendants in lamprey and hagfish, ... responses (EC50s) for skate MR for the mineralocorticoids aldosterone and 11- deoxycorticosterone are 0.07 nM and 0.03 nM, ...
Effect of mineralocorticoid receptor antagonists on proteinuria and progression of chronic kidney disease: a systematic review ... 2016) Effect of mineralocorticoid receptor antagonists on proteinuria and progression of chronic kidney disease: a systematic ... Conclusions: Mineralocorticoid receptor antagonism reduces blood pressure and urinary protein/albumin excretion with a ... Hyperkalaemia is a concern with the use of mineralocorticoid receptor antagonists. We aimed to determine whether the renal ...
Learn and reinforce your understanding of Mineralocorticoids and mineralocorticoid antagonists. ... Mineralocorticoids and mineralocorticoid antagonists Videos, Flashcards, High Yield Notes, & Practice Questions. ... Mineralocorticoid antagonists are drugs that block the action of mineralocorticoids, and they are used to treat conditions such ... mineralocorticoid-receptor agonists, which mimic the role of aldosterone; and mineralocorticoid-receptor antagonists, that ...
The mineralocorticoid receptor (MR) plays an essential role in regulating fluid and electrolyte homeostasis. Amongst ... Myeloid cell-specific ablation of the mineralocorticoid receptor attenuates experimental autoimmune encephalomyelitis. dc. ... Myeloid cell-specific ablation of the mineralocorticoid receptor attenuates experimental autoimmune encephalomyelitis. de. ...
Mineralocorticoids. Class Summary. Replacement of mineralocorticoids is required in patients who have salt-wasting congenital ... Glucocorticoid or mineralocorticoid replacement has no contraindications when it is needed, and it has few drug-drug ... No parenteral form of mineralocorticoid is currently available in the United States; however, if the patient has good GI ... The goal of therapy for adrenal hyperplasia is the replacement of glucocorticoid and mineralocorticoid to prevent signs of ...
Reduced aldosterone production or activity is rare and may be due to congenital or acquired causes.
Mineralocorticoid excess. Presenting features of mineralocorticoid excess include hypertension, headache, tachycardia, fatigue ... Mineralocorticoids (the most important of which is aldosterone), which are secreted by the zona glomerulosa ... Mineralocorticoid replacement is unnecessary in the acute management of acute adrenal insufficiency. Hyperkalemia should be ... Aldosterone accounts for 90% of mineralocorticoid activity, with some activity contributed by deoxycorticosterone, ...
Eplerenone, a mineralocorticoid-receptor antagonist with minimal binding to the progesterone and androgen receptors, is now ... Eplerenone, a mineralocorticoid-receptor antagonist with minimal binding to the progesterone and androgen receptors, is now ... Eplerenone, a mineralocorticoid-receptor antagonist with minimal binding to the progesterone and androgen receptors, is now ... Eplerenone, a mineralocorticoid-receptor antagonist with minimal binding to the progesterone and androgen receptors, is now ...
... Posted on. 2023-08-14. 2023-08-14. Authorlother ... Molecular pharmacology of mineralocorticoid receptor antagonists * Cell types of the heart: identities, interactions, and ... Mineralocorticoid receptor (MR) antagonists have shown remarkable benefits in the treatment of cardiovascular disease. However ... Koca D, Lother A. Molecular pharmacology of mineralocorticoid receptor antagonists: the role of co-regulators. Steroids. 2023: ...
Rat MR(Mineralocorticoid Receptor) ELISA Kit. Rat MR(Mineralocorticoid Receptor) ELISA Kit ... Description: A sandwich ELISA kit for detection of Mineralocorticoid Receptor from Rat in samples from blood, serum, plasma, ... Description: A sandwich ELISA kit for detection of Mineralocorticoid Receptor from Human in samples from blood, serum, plasma, ... The protein functions as a ligand-dependent transcription factor that binds to mineralocorticoid response elements in order to ...
Virtual Forum: Mineralocorticoid receptors & the brain. Posted on. April 12, 2023. April 12, 2023. Authorlother ... April 2023 , Mineralocorticoid receptors & the brain. Onno Meijer, Leiden University, The Netherlands. April 25, 2023, 4 pm CET ... the mineralocorticoid receptor, or related topics worldwide. The forum is open to everybody who is interested upon registration ...
Managing resistant hypertension: focus on mineralocorticoid-receptor antagonists. Overview of attention for article published ...
Geller DS . Mineralocorticoid resistance. Clin Endocrinol (Oxford) 62: 513‐520, 2005.. 108.. Geller DS , Rodriguez‐Soriano J , ... The key mineralocorticoid is aldosterone. Hyperaldosteronism causes sodium and fluid retention in the kidney. Combined with the ... Chronic activation of mineralocorticoid production leads to dysregulation of the cardiovascular system and to hypertension. ... Arriza JL , Weinberger C , Cerelli G , Glaser TM , Handelin BL , Housman DE , Evans RM . Cloning of the human mineralocorticoid ...
Glucocorticoid and mineralocorticoid function. A pathologically low response to the ACTH test was found in 11 of 25 (44%) CF ... Mineralocorticoid insufficiency was not observed in any of the 31 CF patients treated with itraconazole as indicated by normal ... Mineralocorticoid and gonadal insufficiency was not observed in any of the patients. Only one patient with an initial ... In the present study normal plasma-renin levels indicate that no involvement of mineralocorticoid secretion was present in any ...
Vogel S, Klumpers F, Krugers HJ, Fang Z, Oplaat KT, Oitzl MS, Joëls M, Fernández G (2015) Blocking the mineralocorticoid ... ter Horst JP, van der Mark MH, Arp M, Berger S, de Kloet ER, Oitzl MS (2012) Stress or no stress: mineralocorticoid receptors ... van Leeuwen N, Kumsta R, Entringer S, de Kloet ER, Zitman FG, DeRijk RH, Wüst S (2010) Functional mineralocorticoid receptor ( ... van Leeuwen N, Bellingrath S, de Kloet ER, Zitman FG, DeRijk RH, Kudielka BM, Wüst S (2011) Human mineralocorticoid receptor ( ...
mineralocorticoids. *adrenal androgens. *catecholamines, such as:*epinephrine, also known as adrenaline. *norepinephrine ...
Fels, B., Acharya, S., Vahldieck, C., Graf, T., Käding, N., Rupp, J., & Kusche-Vihrog, K. (2022). Mineralocorticoid receptor- ... Fels, B, Acharya, S, Vahldieck, C, Graf, T, Käding, N, Rupp, J & Kusche-Vihrog, K 2022, Mineralocorticoid receptor-antagonism ... Mineralocorticoid receptor-antagonism prevents COVID-19-dependent glycocalyx damage. Benedikt Fels*, Sovon Acharya, Carl ... Mineralocorticoid receptor-antagonism prevents COVID-19-dependent glycocalyx damage. In: Pflugers Archiv European Journal of ...
Regulation of rat mineralocorticoid receptor expression in neurons by progesterone ... Regulation of rat mineralocorticoid receptor expression in neurons by progesterone. Endocrinology, 136, 3800-3806. ...
Mineralocorticoid receptor (MR) pathway activation contributes to diabetic nephropathy but its role in retinopathy is unknown. ... Mineralocorticoid receptor pathway and its antagonism in a model of diabetic retinopathy. ... The sustained intraocular delivery of spironolactone, a steroidal mineralocorticoid antagonist, decreased the early and late ...
Is the mineralocorticoid receptor in Brown Norway rats constitutively active?. N. Marissal-Arvy, E. Ribot, A. Sarrieau, P. ...
Effects of Glucocorticoid Hormones on Pain Sensitivity: Involvement of Glucocorticoid and Mineralocorticoid Receptors *N. I. ...
Mineralocorticoid signaling in transition to heart failure with normal ejection fraction. Brian P. Shapiro, Theophilus E. Owan ... Mineralocorticoid signaling in transition to heart failure with normal ejection fraction. / Shapiro, Brian P.; Owan, Theophilus ... Mineralocorticoid signaling in transition to heart failure with normal ejection fraction. In: Hypertension. 2008 ; Vol. 51, No ... Shapiro, BP, Owan, TE, Mohammed, S, Kruger, M, Linke, WA, Burnett, JC & Redfield, MM 2008, Mineralocorticoid signaling in ...
Corticosteroids and mineralocorticoids. *Ephedra and many other herbal products. *Erythropoietin. *Estrogens (including birth ...
Different isozymes of mouse 11/β-hydroxylase produce mineralocorticoids and glucocorticoids. Leslie J. Domalik, David D. ... Different isozymes of mouse 11/β-hydroxylase produce mineralocorticoids and glucocorticoids. Molecular Endocrinology. 1991 Dec; ... Different isozymes of mouse 11/β-hydroxylase produce mineralocorticoids and glucocorticoids. In: Molecular Endocrinology. 1991 ... Different isozymes of mouse 11/β-hydroxylase produce mineralocorticoids and glucocorticoids. / Domalik, Leslie J.; Chaplin, ...
Stress Induces a Shift Towards Striatum-Dependent Stimulus-Response Learning via the Mineralocorticoid Receptor *Susanne Vogel ...
30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor activation and specificity-conferring mechanisms: a ... The mineralocorticoid receptor (MR) was first characterized 45 years ago (Funder 1972, Rousseau 1972), a decade and a half ...

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