Aldosterone: 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.Aldosterone Synthase: 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.Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.Receptors, Mineralocorticoid: 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.Spironolactone: 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)Hyperaldosteronism: A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.Renin: 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.Mineralocorticoids: 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.Zona Glomerulosa: The narrow subcapsular outer zone of the adrenal cortex. This zone produces a series of enzymes that convert PREGNENOLONE to ALDOSTERONE. The final steps involve three successive oxidations by CYTOCHROME P-450 CYP11B2.Steroid 11-beta-Hydroxylase: 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).Adrenal Glands: 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.Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.Angiotensin II: 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.Adrenalectomy: Excision of one or both adrenal glands. (From Dorland, 28th ed)Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity.Renin-Angiotensin System: 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.18-Hydroxycorticosterone: 11 beta,18,21-Trihydroxypregn-4-ene-3,20-dione.Adrenal Cortex: 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.Canrenoic Acid: A synthetic pregnadiene derivative with anti-aldosterone activity.Potassium: 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.11-beta-Hydroxysteroid Dehydrogenase Type 2: 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.Epithelial Sodium Channels: 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.Adrenocorticotropic Hormone: 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).Kidney Tubules, Collecting: 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.Hypertension: 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.Hydrocortisone: 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.Diet, Sodium-Restricted: A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)Corticosterone: 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)Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Sodium, Dietary: Sodium or sodium compounds used in foods or as a food. The most frequently used compounds are sodium chloride or sodium glutamate.Desoxycorticosterone: A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.Hypokalemia: 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)Kidney Tubules, Distal: 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.18-Hydroxydesoxycorticosterone: An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.Amiloride: 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)Sodium Chloride, Dietary: Sodium chloride used in foods.Canrenone: A synthetic pregnadiene compound with anti-aldosterone activity.Electrolytes: 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)Diuretics: Agents that promote the excretion of urine through their effects on kidney function.Adrenal Cortex Neoplasms: Tumors or cancers of the ADRENAL CORTEX.Hypoaldosteronism: A congenital or acquired condition of insufficient production of ALDOSTERONE by the ADRENAL CORTEX leading to diminished aldosterone-mediated synthesis of Na(+)-K(+)-EXCHANGING ATPASE in renal tubular cells. Clinical symptoms include HYPERKALEMIA, sodium-wasting, HYPOTENSION, and sometimes metabolic ACIDOSIS.Water-Electrolyte Balance: 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.Natriuresis: Sodium excretion by URINATION.Adrenocortical Adenoma: A benign neoplasm of the ADRENAL CORTEX. It is characterized by a well-defined nodular lesion, usually less than 2.5 cm. Most adrenocortical adenomas are nonfunctional. The functional ones are yellow and contain LIPIDS. Depending on the cell type or cortical zone involved, they may produce ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE.Atrial Natriuretic Factor: A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.Adrenal Gland Neoplasms: Tumors or cancer of the ADRENAL GLANDS.Sodium Chloride Symporters: 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.Sodium Chloride: A ubiquitous sodium salt that is commonly used to season food.Dexamethasone: An anti-inflammatory 9-fluoro-glucocorticoid.Sodium Channels: 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.Receptors, Glucocorticoid: 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.Rats, Sprague-Dawley: 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.Potassium, Dietary: Potassium or potassium compounds used in foods or as foods.Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.Hyperkalemia: 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)Vasopressins: Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.Fadrozole: A selective aromatase inhibitor effective in the treatment of estrogen-dependent disease including breast cancer.Potassium Deficiency: A condition due to decreased dietary intake of potassium, as in starvation or failure to administer in intravenous solutions, or to gastrointestinal loss in diarrhea, chronic laxative abuse, vomiting, gastric suction, or bowel diversion. Severe potassium deficiency may produce muscular weakness and lead to paralysis and respiratory failure. Muscular malfunction may result in hypoventilation, paralytic ileus, hypotension, muscle twitches, tetany, and rhabomyolysis. Nephropathy from potassium deficit impairs the concentrating mechanism, producing POLYURIA and decreased maximal urinary concentrating ability with secondary POLYDIPSIA. (Merck Manual, 16th ed)Angiotensin II Type 1 Receptor Blockers: Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.Diuresis: An increase in the excretion of URINE. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.11-beta-Hydroxysteroid Dehydrogenases: 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.RNA, Messenger: 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.Glycyrrhiza: A genus of leguminous herbs or shrubs whose roots yield GLYCYRRHETINIC ACID and its derivative, CARBENOXOLONE.Hydroxysteroid Dehydrogenases: Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.TetrazolesCaptopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.Kidney Cortex: The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Receptor, Angiotensin, Type 1: An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Stimulation, Chemical: The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.Cells, Cultured: 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.Peptidyl-Dipeptidase A: A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC 3.4.15.1.Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.

Acute and chronic dose-response relationships for angiotensin, aldosterone, and arterial pressure at varying levels of sodium intake. (1/2815)

We examined the acute and chronic dose-response relationships between intravenously infused angiotensin II (A II) and the resulting changes in arterial pressure and plasma aldosterone concentration at varying levels of sodium intake. Sequential analysis of plasma aldosterone at each A II infusion rate resulted in an acute dose-related increase in plasma aldosterone which was markedly attenuated after the first 24 hours of infusion, the final level being directly related to the dose of A II and inversely related to sodium intake. A II infused at 5,15, and 23 ng/kg per min was associated with an initial increase (2nd to 8th hour) in plasma aldosterone to 2,6, and 9 times control values, respectively, in dogs receiving 40 mEq Na+/day. But, after the 1st day, aldosterone averaged only 1, 1.7, and 3 times control values for the next 2 weeks at the same rates of A II infusion. Dogs receiving 120 mEq Na+/day during A II infusion exhibited only a transient increase in plasma aldosterone during the 1st day. Sustained hypertension developed over a period of a week at all doses of A II at normal and high sodium intake, but did not occur at any dose of A II in sodium-depleted dogs. Increasing sodium intake from 40 to 120 mEq/day resulted in higher levels of hypertension, 125% compared to 140% of ocntrol values for dogs infused with A II, 5.0 ng/kg per min. We conclude that primary angiotensin-induced hypertension need not be associated with increased levels of plasma aldosterone, which appears to remain elevated only with amounts of A II greater than those required to sustain a significant degree of hypertension.  (+info)

Low calorie diet enhances renal, hemodynamic, and humoral effects of exogenous atrial natriuretic peptide in obese hypertensives. (2/2815)

The expression of the natriuretic peptide clearance receptor is abundant in human and rat adipose tissue, where it is specifically inhibited by fasting. In obese hypertensives, plasma atrial natriuretic peptide (ANP) levels were found to be lower than in obese normotensives. Therefore, the increased adipose mass might influence ANP levels and/or its biological activity. The aim of the present study was to evaluate whether the humoral, hemodynamic, and renal effects of exogenous ANP in obese hypertensives might be enhanced by a very low calorie diet. Eight obese hypertensives received a bolus injection of ANP (0.6 mg/kg) after 2 weeks of a normal calorie/normal sodium diet, and blood pressure (BP), heart rate, ANP, cGMP, plasma renin activity, and aldosterone were evaluated for 2 hours before and after the injection. Diuresis and natriuresis were measured every 30 minutes. The patients then started a low calorie/normal sodium diet (510 kcal/150 mmol/d) for 4 days, and then the ANP injection protocol was repeated. The low calorie diet induced a slight weight loss (from 90.6+/-1.1 to 87. 7+/-1.2 kg; P<0.01), which was accompanied by increase of cGMP excretion (from 146.0+/-10.1 to 154.5+/-9.5 nmol/24 h; P<0.05) together with a reduction of BP (P<0.01 versus basal levels). ANP injection after diet was followed by an increase of ANP levels similar to that observed before diet, but plasma cGMP, diuresis, and natriuresis increased significantly only after diet. Similarly, the decrease of BP after ANP administration was significantly higher after diet (change in mean arterial pressure, -6.4+/-0.7 versus -4. 0+/-0.6 mm Hg; P<0.05) as well as that of aldosterone (P<0.01). These data show that a low calorie diet enhances the humoral, renal, and hemodynamic effects of ANP in obese hypertensives and confirm the importance of caloric intake in modulating the biological activity of ANP, suggesting that the natriuretic peptide system can play a role in the acute changes of natriuresis and diuresis associated with caloric restriction.  (+info)

Aldosterone excretion rate and blood pressure in essential hypertension are related to polymorphic differences in the aldosterone synthase gene CYP11B2. (3/2815)

Significant correlation of body sodium and potassium with blood pressure (BP) may suggest a role for aldosterone in essential hypertension. In patients with this disease, the ratio of plasma renin to plasma aldosterone may be lower than in control subjects and plasma aldosterone levels may be more sensitive to angiotensin II (Ang II) infusion. Because essential hypertension is partly genetic, it is possible that altered control of aldosterone synthase gene expression or translation may be responsible. We compared the frequency of 2 linked polymorphisms, one in the steroidogenic factor-1 (SF-1) binding site and the other an intronic conversion (IC), in groups of hypertensive and normotensive subjects. In a larger population, the relationship of aldosterone excretion rate to these polymorphisms was also evaluated. In 138 hypertensive subjects, there was a highly significant excess of TT homozygosity (SF-1) over CC homozygosity compared with a group of individually matched normotensive control subjects. The T allele was significantly more frequent than the C allele in the hypertensive group compared with the control group. Similarly, there was a highly significant relative excess of the conversion allele over the "wild-type" allele and of conversion homozygosity over wild-type homozygosity in the hypertensive group compared with the control group. In 486 subjects sampled from the North Glasgow Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) population, SF-1 and IC genotypes were compared with tetrahydroaldosterone excretion rate. Subjects with the SF-1 genotypes TT or TC had significantly higher excretion rates than those with the CC genotype. The T allele was associated with higher excretion rates than the C allele. However, no significant differences were found in excretion rate between subjects of different IC genotype. Urinary aldosterone excretion rate may be a useful intermediate phenotype linking these genotypes to raised BP. However, no causal relationship has yet been established, and it is possible that the polymorphisms may be in linkage with other causative mutations.  (+info)

Sodium requirement of adult cats for maintenance based on plasma aldosterone concentration. (4/2815)

The sodium requirement of adult cats for maintenance was determined using a randomized block design of eight dietary sodium treatments (0.1, 0.4, 0.5, 0.66, 0.8, 1.2, 1.6 or 2.0 g Na/kg in a casein-lactalbumin-based purified diet) administered for periods of 4 wk. A total of 35 adult specific-pathogen-free domestic shorthaired cats (26 males and 9 females, 1.5-3 y of age) was given an equilibration diet (2 g Na/kg) for 14 d before assignment (or reassignment) to the treatments. A total of 12 cats (8 males, 4 females) was randomly assigned to the lowest six levels of sodium, and four cats to the highest two sodium levels. Cats consuming the diet containing 0.1 g Na/kg had significantly elevated aldosterone concentration in plasma, and packed cell volume. In addition, these cats exhibited anorexia, body weight loss, reduced urinary specific gravity and sodium excretion, and had a negative sodium balance. However, adult cats did not develop polydypsia and polyuria reported in sodium-deficient kittens. Cats given the diet containing 0.66 g Na/kg did not have an increased packed cell volume, but aldosterone concentration in the plasma was significantly elevated. However, cats given diets containing >/=0.8 g Na/kg had plasma aldosterone concentrations +info)

Epithelial sodium channel regulated by aldosterone-induced protein sgk. (5/2815)

Sodium homeostasis in terrestrial and freshwater vertebrates is controlled by the corticosteroid hormones, principally aldosterone, which stimulate electrogenic Na+ absorption in tight epithelia. Although aldosterone is known to increase apical membrane Na+ permeability in target cells through changes in gene transcription, the mechanistic basis of this effect remains poorly understood. The predominant early effect of aldosterone is to increase the activity of the epithelial sodium channel (ENaC), although ENaC mRNA and protein levels do not change initially. Rather, the open probability and/or number of channels in the apical membrane are greatly increased by unknown modulators. To identify hormone-stimulated gene products that modulate ENaC activity, a subtracted cDNA library was generated from A6 cells, a stable cell line of renal distal nephron origin, and the effect of candidates on ENaC activity was tested in a coexpression assay. We report here the identification of sgk (serum and glucocorticoid-regulated kinase), a member of the serine-threonine kinase family, as an aldosterone-induced regulator of ENaC activity. sgk mRNA and protein were strongly and rapidly hormone stimulated both in A6 cells and in rat kidney. Furthermore, sgk stimulated ENaC activity approximately 7-fold when they were coexpressed in Xenopus laevis oocytes. These data suggest that sgk plays a central role in aldosterone regulation of Na+ absorption and thus in the control of extracellular fluid volume, blood pressure, and sodium homeostasis.  (+info)

Primary aldosteronism with aldosterone-producing adrenal adenoma in a pregnant woman. (6/2815)

A 30-year-old pregnant woman complained of muscle weakness at 29 weeks' gestation. She was hypertensive with severe hypokalemia. Lower plasma renin activity and higher aldosterone level than the normal values in pregnancy suggested primary aldosteronism. A cesarean delivery was performed at 31 weeks' gestation because of pulmonary congestion. The neonatal course was uncomplicated. The laparoscopic adrenalectomy for a 2.0-cm right adrenal adenoma resulted in normalizing of her blood pressure and serum potassium level. Although primary aldosteronism is rare, especially during pregnancy, it should be always considered as one of etiologies of hypertension in pregnancy.  (+info)

Aldosterone, not estradiol, is the physiological agonist for rapid increases in cAMP in vascular smooth muscle cells. (7/2815)

BACKGROUND: Steroid-induced gene regulation in the endocrine tissues and vascular wall is achieved through the interaction of specific receptor proteins and promoters of target genes. In addition to these delayed steroid actions, rapid effects of steroids have been reported in various tissues that were clearly incompatible with the classic theory of genomic steroid action. METHODS AND RESULTS: Because high doses of 17beta-estradiol have been shown to modulate intracellular cAMP levels in vascular smooth muscle cells, steroid-induced stimulation of adenylate cyclase stimulation and phosphorylation of cAMP response element binding protein was investigated in porcine coronary artery vascular smooth muscle cells. Aldosterone induces a approximately 1.5- to 2.5-fold increase in intracellular cAMP levels (EC50 approximately 0.01 to 0.1 nmol/L) within 1 minute, whereas 17beta-estradiol and hydrocortisone act only at supraphysiological concentrations (10 micromol/L). Aldosterone-induced changes in intracellular cAMP are calcium dependent; they are not blocked by inhibitors of mineralocorticoid receptors, transcription, or protein synthesis. In addition, aldosterone induces a time-dependent phosphorylation of cAMP response element binding protein with potential transcriptional importance. CONCLUSIONS: A nongenomic modulation of vascular smooth muscle cells by aldosterone is consistent with the data that aldosterone, not estrogen, is the physiological stimulus for cAMP.  (+info)

Comparison of two aquaretic drugs (niravoline and OPC-31260) in cirrhotic rats with ascites and water retention. (8/2815)

kappa-Opioid receptor agonists (niravoline) or nonpeptide antidiuretic hormone (ADH) V2 receptor antagonists (OPC-31260) possess aquaretic activity in cirrhosis; however, there is no information concerning the effects induced by the chronic administration of these drugs under this condition. To compare the renal and hormonal effects induced by the long-term oral administration of niravoline, OPC-31260, or vehicle, urine volume, urinary osmolality, sodium excretion, and urinary excretion of aldosterone (ALD) and ADH were measured in basal conditions and for 10 days after the daily oral administration of niravoline, OPC-31260, or vehicle to cirrhotic rats with ascites and water retention. Creatinine clearance, serum osmolality, ADH mRNA expression, and systemic hemodynamics were also measured at the end of the study. Niravoline increased water excretion, peripheral resistance, serum osmolality, and sodium excretion and reduced creatinine clearance, ALD and ADH excretion, and mRNA expression of ADH. OPC-31260 also increased water metabolism and sodium excretion and reduced urinary ALD, although the aquaretic effect was only evident during the first 2 days, and no effects on serum osmolality, renal filtration, and systemic hemodynamics were observed. Therefore, both agents have aquaretic efficacy, but the beneficial therapeutic effects of the long-term oral administration of niravoline are more consistent than those of OPC-31260 in cirrhotic rats with ascites and water retention.  (+info)

1. Intra-erythrocyte sodium, potassium, ATP and (Na+,K+-activated)-ATPase concentrations and urinary aldosterone excretion were compared in 3-month-old spontaneously hypertensive rats (n = 11) and normotensive Wistar-Kyoto control rats (n = 11).. 2. Spontaneously hypertensive rats exhibited significantly higher intra-erythrocyte sodium concentration (5.5 ± 1.3 vs 4.0 ± 1.1 mmol/l of erythrocytes, P , 0.01). No significant difference was found in intra-erythrocyte potassium, ATP or (Na+,K+-activated)-ATPase concentration.. 3. Mean urinary aldosterone excretion was significantly lower in spontaneously hypertensive rats (66.3 ± 6.5 pmol/24 h) than in Wistar-Kyoto rats (90.5 ± 10.6 pmol/24 h, P , 0.01). No significant relationship between urinary aldosterone and intra-erythrocyte sodium concentration was found in spontaneously hypertensive or Wistar-Kyoto rats or in the pooled group.. 4. These results are thus consistent with previous findings of an increased intracellular sodium concentration ...
CONTEXT: Body mass index (BMI) shows a direct correlation with plasma aldosterone concentration (PAC) and urinary aldosterone excretion in normotensive individuals; whether the same applies to hypertensive patients is unknown. OBJECTIVE: Our objective was to determine if BMI predicts PAC and the PAC/plasma renin activity ratio [aldosterone renin ratio (ARR)] in hypertensive patients, and if this affects the identification of primary aldosteronism (PA). DESIGN: This was a prospective evaluation of consecutive hypertensive patients referred nationwide to specialized hypertension centers. MAIN OUTCOME MEASURES: Sitting PAC, plasma renin activity, and the ARR, baseline and after 50 mg captopril orally with concomitant assessment of parameters, including BMI and daily sodium intake, were calculated. RESULTS: Complete biochemical data and a definite diagnosis were obtained in 1125 consecutive patients. Of them 999 had primary (essential) hypertension (PH) and 126 (11.2%) PA caused by an ...
In the first part of this study, we showed that UAE in patients with aldosterone escape is significantly higher than that in patients without. In the second part, although our data were obtained in a small sample, we demonstrated that adding spironolactone to treatment of with an ACE inhibitor is clinically useful and safe for patients with aldosterone escape.. Three aspects of this study are worthy of analysis. One is that aldosterone escape was detected in 40% of patients with early diabetic nephropathy. Escape of aldosterone production despite ACE inhibition has been shown in patients with hypertension,6,21,22 chronic heart failure,4,23 and in those with acute myocardial infarction.24 We have previously shown that aldosterone escape during ACE inhibition treatment occurred in 46% of patients with essential hypertension6 and to a very similar extent to that in the present study. In terms of the mechanisms of aldosterone escape, we previously reported that changes in blood pressure, ...
Excessive activation of β-adrenergic, angiotensin II, and aldosterone signaling pathways promotes mortality after myocardial infarction (MI), while antagonist drugs targeting these pathways are core therapies for treating post-MI patients. The multifunctional calcium/calmodulin-dependent protein kinase II (CaMKII) is activated by catecholamines and angiotensin II, and CaMKII inhibition prevents isoproterenol- and angiotensin II-mediated cardiomyopathy. Here we ask the hypothesis if aldosterone and CaMKII participated in common responses to MI by developing a mouse MI model supplemented by aldosterone infusion (MI+Aldo) to approximate plasma aldosterone levels measured in MI patients. We find that aldosterone exerts direct toxic actions on myocardium by oxidative activation of CaMKII, causing cardiac rupture and increased mortality in mice after MI (65.5% for aldosterone versus 31.0% for vehicle, P=0.007, n≥19 mice per treatment). Aldosterone oxidizes CaMKII by recruiting NADPH oxidase, and ...
Circulating aldosterone levels are increased in human pregnancy. Inadequately low aldosterone levels as present in preeclampsia, a life-threatening disease for both mother and child, are discussed to be involved in its pathogenesis or severity. Moreover, inactivating polymorphisms in the aldosterone synthase gene have been detected in preeclamptic women. Here, we used aldosterone synthase-deficient (AS(-/-)) mice to test whether the absence of aldosterone is sufficient to impair pregnancy or even to cause preeclampsia. AS(-/-) and AS(+/+) females were mated with AS(+/+) and AS(-/-) males, respectively, always generating AS(+/-) offspring. With maternal aldosterone deficiency in AS(-/-) mice, systolic blood pressure was low before and further reduced during pregnancy with no increase in proteinuria. Yet, AS(-/-) had smaller litters due to loss of fetuses as indicated by a high number of necrotic placentas with massive lymphocyte infiltrations at gestational day 18. Surviving fetuses and their ...
1. The effect of intravenous loading with 500 ml of sodium chloride solution (50 g/l) on plasma renin concentration, plasma aldosterone concentration, urinary sodium excretion and mean blood pressure was studied in 15 young patients with mild essential hypertension and 10 healthy normotensive control subjects.. 2. Plasma renin concentration and plasma aldosterone concentration were suppressed to the same degree during loading in both the hypertensive and normotensive groups. Urinary sodium excretion was significantly higher in the hypertensive patients than in the normotensive subjects. Mean blood pressure increased slightly in both groups.. 3. Plasma renin concentration and plasma aldosterone concentration were significantly correlated in both groups before sodium loading. The increase in urinary sodium excretion was significantly correlated to the suppression of plasma aldosterone concentration in the hypertensive, but not in the normotensive, group. No correlation was found between changes in ...
Our cross-sectional analysis indicated a positive association between plasma aldosterone levels and insulin resistance. However, this association may be an epiphenomenon. Accordingly, we hypothesized that high levels of plasma aldosterone could predict the development of insulin resistance. Our results confirmed the hypothesis in subjects without insulin resistance at baseline. Although a recent prospective study from the Framingham Offspring Study29 has demonstrated that higher aldosterone levels are associated with the development of metabolic syndrome, they failed to demonstrate the association of aldosterone with the development of insulin resistance. The reason was not clear, but they stated in their limitations that, for the calculation of HOMA-insulin resistance, they used glucose and insulin 4 years before the baseline examination. Another explanation may be the racial difference, including the demographic backgrounds of the subjects, such as the prevalence of obesity; mean BMI in the ...
1. Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats.. 2. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 ...
The effects of retinoids on adrenal aldosterone synthase gene (CYP11B2) expression and aldosterone secretion are still unknown. We therefore examined the effects of nuclear retinoid X receptor (RXR) pan-agonist PA024 on CYP11B2 expression, aldosterone secretion and blood pressure, to elucidate its potential as a novel anti-hypertensive drug. We demonstrated that PA024 significantly suppressed angiotensin II (Ang II)-induced CYP11B2 mRNA expression, promoter activity and aldosterone secretion in human adrenocortical H295R cells. Human CYP11B2 promoter functional analyses using its deletion and point mutants indicated that the suppression of CYP11B2 promoter activity by PA024 was in the region from -1521 (full length) to -106 including the NBRE-1 and the Ad5 elements, and the Ad5 element may be mainly involved in the PA024-mediated suppression. PA024 also significantly suppressed the Ang II-induced mRNA expression of transcription factors NURR1 and NGFIB that bind to and activate the Ad5 element. ...
The classic renin-angiotensin system is partly responsible for controlling aldosterone secretion from the adrenal cortex via the peptide angiotensin II (AngII). In addition, there is a local adrenocortical renin-angiotensin system that may be involved in the control of aldosterone synthesis in the zona glomerulosa (ZG). In order to characterize the long-term control of adrenal steroidogenesis, we utilized adrenal glands from renin knockout (KO) rats and compared steroidogenesis in vitro and steroidogenic enzyme expression to wild-type (WT) controls (Dahl S rat). Adrenal capsules (ZG; aldosterone production) and subcapsules (zona reticularis/fasciculata [ZFR]; corticosterone production) were separately dispersed and studied in vitro. Plasma renin activity and angiotensin II concentrations were extremely low in the KO rats. Basal and cAMP-stimulated aldosterone production was significantly reduced in renin KO ZG cells whereas corticosterone production was not different between WT and KO ZFR cells. As
It is 10 years since Davis and his associates have shown that decapitation of hypophysectomized dogs does not alter aldosterone secretion nor prevent a marked increase in aldosterone output in response to hemorrhage. Since then it has been popularly assumed that the reninangiotensin system is the primary regulator of aldosterone secretion. This issue is not yet settled satisfactorily, however. Whereas in man and experimental animals aldosterone secretion continues in the complete absence of the pituitary glands, many investigators have found that hypophysectomy or spontaneous hyperpituitarism results in an impaired aldosterone secretion under basal conditions or under various physiological stimuli. ...
Local resource for aldosterone therapy in Casper. Includes detailed information on local businesses that provide access to hormone replacement, chronic aldosterone therapy, aldosterone replacement therapy, HRT therapy, and natural hormone therapy, as well as advice and content on bioidentical hormones.
Local resource for aldosterone therapy in Waterloo. Includes detailed information on local businesses that provide access to hormone replacement, chronic aldosterone therapy, aldosterone replacement therapy, HRT therapy, and natural hormone therapy, as well as advice and content on bioidentical hormones.
The major findings of the present study are as follows: (1) AT1A-KO mice with MI had cardiac hypertrophy, cardiac dysfunction, and collagen gene expression, along with increased cardiac expression of the CYP11B2 gene and elevated cardiac aldosterone levels. (2) Spironolactone administration inhibited LV remodeling and resulted in almost normalized LV geometry, as well as reversing altered cardiac gene expressions (ANP, BNP, type I and type III collagens) in AT1A-KO MI mice. These results suggest that aldosterone is produced via an Ang II-independent mechanism in hearts with MI and that it promotes cardiac hypertrophy, fibrosis, and subsequent heart failure after MI.. Several regulators are known to stimulate aldosterone synthesis in the adrenal cortex, including Ang II, corticotropin, and plasma concentrations of Na+ and/or K+. Among these, Ang II is the primary physiological regulator because it is well known that blockade of the renin-angiotensin system by ACE inhibitors or Ang II receptor ...
I recently had my aldosterone and renin checked. The results were: Aldosterone 17.2, Renin 0.1, Aldosterone/Renin Ratio 172.0. For years Ive had low potassium and taking a potassium prescription whic...
Accumulating evidence suggests that the nongenomic cardiovascular actions of aldosterone are produced by varied cellular pathways and mediated by a multitude of messenger systems including the reactive oxygen and nitrogen species. Considering the involvement of the oxidative and nitrosative stress in the pathways leading to the activation of the angiotensin - aldosterone system, in the current study we tried to evaluate the functional interactions between aldosterone, angiotensin II and antioxidants in isolated vascular smooth muscle of aortic rings from rats. Our data provide additional arguments that the nongenomic actions of aldosterone on aortic smooth muscle cells of rats are a question of cross-talk and balance between its rapid vasoconstrictor and vasodilator effects, as result of the activation of reactive oxygen species in the first case and of nitrogen species in the second. In this way, it seems that at low ambient oxidative stress, aldosterone promotes nitric oxide (NO) production ...
The toxic effects of aldosterone on the vasculature, and in particular on the endothelial layer, have been proposed as having an important role in the cardiovascular pathology observed in mineralocorticoid-excess states. In order to characterize the genomic molecular mechanisms driving the aldosterone-induced endothelial dysfunction, we performed an expression microarray on transcripts obtained from both human umbilical vein endothelial cells and human coronary artery endothelial cells stimulated with 10 - 7 M aldosterone for 18 h. The results were then subjected to qRT-PCR confirmation, also including a group of genes known to be involved in the control of the endothelial function or previously described as regulated by aldosterone. The state of activation of the mineralocorticoid receptor was investigated by means of a luciferase-reporter assay using a plasmid encoding a mineralocorticoid and glucocorticoid-sensitive promoter. Aldosterone did not determine any significant change in gene ...
Aims Accurate serum aldosterone determination is critical to the screening and diagnosis of primary aldosteronism, the localisation of aldosterone producing tumours, and the investigation of other disorders of the renin-angiotensin system. Mass spectrometry offers a means to overcome problems with method-dependent bias between competitive immunoassays for aldosterone. The authors have developed a simple, sensitive and precise liquid-liquid extraction aldosterone method for the ABSCIEX API-5000 liquid chromatography and tandem mass spectrometry (LC-MS/MS) system. ...
The mineralocorticoid aldosterone is produced in the adrenal zona glomerulosa (ZG) under the control of the renin-angiotensin II (AngII) system. Primary aldosteronism (PA) results from renin-independent production of aldosterone and is a common cause of hypertension. PA is caused by dysregulated localization of the enzyme aldosterone synthase (Cyp11b2), which is normally restricted to the ZG. Cyp11b2 transcription and aldosterone production are predominantly regulated by AngII activation of the Gq signaling pathway. Here, we report the generation of transgenic mice with Gq-coupled designer receptors exclusively activated by designer drugs (DREADDs) specifically in the adrenal cortex. We show that adrenal-wide ligand activation of Gq DREADD receptors triggered disorganization of adrenal functional zonation, with induction of Cyp11b2 in glucocorticoid-producing zona fasciculata cells. This result was consistent with increased renin-independent aldosterone production and hypertension. All ...
The mineralocorticoid aldosterone is produced in the adrenal zona glomerulosa (ZG) under the control of the renin-angiotensin II (AngII) system. Primary aldosteronism (PA) results from renin-independent production of aldosterone and is a common cause of hypertension. PA is caused by dysregulated localization of the enzyme aldosterone synthase (Cyp11b2), which is normally restricted to the ZG. Cyp11b2 transcription and aldosterone production are predominantly regulated by AngII activation of the Gq signaling pathway. Here, we report the generation of transgenic mice with Gq-coupled designer receptors exclusively activated by designer drugs (DREADDs) specifically in the adrenal cortex. We show that adrenal-wide ligand activation of Gq DREADD receptors triggered disorganization of adrenal functional zonation, with induction of Cyp11b2 in glucocorticoid-producing zona fasciculata cells. This result was consistent with increased renin-independent aldosterone production and hypertension. All ...
Essential hypertension is seen as a contemporary public health challenge not only because of its high prevalence and variable treatment response but also because it represents a major risk factor for cardiovascular disease. Both genetic and environmental factors contribute to the regulation of blood pressure, thus making the study of hypertension difficult and complex. Over recent years, with the advent of new molecular technologies, there has been an increasing interest in its genetic component. Alterations in the rate and pattern of adrenal steroid biosynthesis can contribute to blood pressure changes and its heritable component. In humans, mutations in the genes encoding aldosterone synthase (CYP11B2) and 11β-hydroxylase (CYP11B1), responsible for the final stages of aldosterone and cortisol production respectively, lead to rare monogenic disorders. Both, glucocorticoid remediable aldosteronism and 11β-hydroxylase deficiency are associated with mineralocorticoid hypertension. More subtle ...
1. The effect of 5 consecutive days of hill walking on electrolyte balance, fluid homeostasis, plasma renin activity and plasma aldosterone concentration was studied in five male subjects.. 2. The 5-day exercise period was preceded by a 4-day control period and followed by a 4-day recovery period. Throughout the 13-day study subjects ate a fixed diet.. 3. After 5 days of exercise subjects had retained a mean of 264 mmol (sd 85) of sodium. Plasma sodium concentration remained constant at 142.0 mmol/l (sd 5.4). This indicates an expansion of the extracellular space by 1.84 litres.. 4. By the end of the exercise period there was a positive water balance of about 0.9 litre. Thus there was a net movement of 0.94 litre of fluid from the intracellular to the extracellular space.. 5. Packed cell volume decreased from a mean of 43.5% to 37.9% after 5 days of exercise, indicating that about 0.9 litre of the extracellular fluid entered the vascular compartment. The remaining fluid may be responsible for ...
Approximately 1-2% of individuals with primary hypertension have primary hyperaldosteronism characterized by hypokalemia (low potassium) and low direct renin. Because serum aldosterone concentrations vary due to dietary sodium intake and body position, some physicians prefer measurement of 24-hour urine concentrations for aldosterone ...
Aldosterone-producing adenomas (APAs) are benign tumors of the adrenal gland that constitutively produce the salt-retaining steroid hormone aldosterone and cause millions of cases of severe hypertension worldwide. Either of 2 somatic mutations in the potassium channel KCNJ5 (G151R and L168R, hereafter referred to as KCNJ5MUT) in adrenocortical cells account for half of APAs worldwide. These mutations alter channel selectivity to allow abnormal Na+ conductance, resulting in membrane depolarization, calcium influx, aldosterone production, and cell proliferation. Because APA diagnosis requires a difficult invasive procedure, patients often remain undiagnosed and inadequately treated. Inhibitors of KCNJ5MUT could allow noninvasive diagnosis and therapy of APAs carrying KCNJ5 mutations. Here, we developed a high-throughput screen for rescue of KCNJ5MUT-induced lethality and identified a series of macrolide antibiotics, including roxithromycin, that potently inhibit KCNJ5MUT, but not KCNJ5WT. ...
Aldosterone-producing adenomas (APAs) are benign tumors of the adrenal gland that constitutively produce the salt-retaining steroid hormone aldosterone and cause millions of cases of severe hypertension worldwide. Either of 2 somatic mutations in the potassium channel KCNJ5 (G151R and L168R, hereafter referred to as KCNJ5MUT) in adrenocortical cells account for half of APAs worldwide. These mutations alter channel selectivity to allow abnormal Na+ conductance, resulting in membrane depolarization, calcium influx, aldosterone production, and cell proliferation. Because APA diagnosis requires a difficult invasive procedure, patients often remain undiagnosed and inadequately treated. Inhibitors of KCNJ5MUT could allow noninvasive diagnosis and therapy of APAs carrying KCNJ5 mutations. Here, we developed a high-throughput screen for rescue of KCNJ5MUT-induced lethality and identified a series of macrolide antibiotics, including roxithromycin, that potently inhibit KCNJ5MUT, but not KCNJ5WT. ...
The response of plasma aldosterone (PA) and plasma renin activity (PRA) to ACTH stimulation (0.25 mg Tetracosactide infusion/10 h) and to insulin-induced hypoglycemia (0.1 U/kg b.w.) has been studied in 34 essential hypertensive (EH) patients. Corticotrophin stimulation increases significantly PA, the percent increase being higher in normal PRA EH patients than in controls but comparable to controls in low PRA EH patients. PRA shows a slight and transient elevation. A significant increase in PA is observed also during the insulin test, but the percent increase is lower than that under ACTH stimulation. The possibility that aldosterone is involved, under severe and frequent stress, in the genesis of essential hypertension is discussed.
Hypertension, or high blood pressure, is a common disorder. The underlying cause of hypertension is, as yet, unidentified. Many researchers believe an expansion of blood volume precedes the rise in blood pressure. Aldosterone, an important regulator of blood volume, is produced in the outermost layer of the adrenal cortex. Aldosterone promotes the reabsorption of sodium ions (Na+) from kidney tubules back into the blood. Since water is reabsorbed with sodium, aldosterone increases blood volume and blood pressure. The role of aldosterone in hypertension has been studied using receptor blocking agents, or complete adrenalectomy, (removal of both adrenal glands), with each method resulting in confounding variables. A surgically-induced low-aldosterone state has been developed in this laboratory. The process involves removal of one adrenal gland, and cryo-destruction of the outer layer of the remaining gland. This procedure markedly reduces aldosterone levels, while maintaining the production of the other
Aldosterone, also known as aldocorten or delta-aldosterone, belongs to the class of organic compounds known as 21-hydroxysteroids. These are steroids carrying a hydroxyl group at the 21-position of the steroid backbone. Aldosterone exists as a solid, possibly soluble (in water), and an extremely weak basic (essentially neutral) compound (based on its pKa) molecule. Aldosterone exists in all living organisms, ranging from bacteria to humans ...
Aldosterone is a major regulator of Na+-absorptive and K+-secretory processes in the distal segment of mammalian colon. In this study, the distribution of aldosterone-sensitive cell types in isolated rat distal colon was determined using site-directed intracellular microelectrodes, specific Na+- and K+-channel blockers, and aldosterone-receptor binding techniques. Electrophysiological data indicated that aldosterone induced parallel apical membrane Na+ and K+ conductances, mainly in surface cells and to a significantly lesser degree in crypt cells. Scatchard analyses of aldosterone-receptor binding in cytosolic fractions revealed the maximum number of specific binding sites in whole mucosal homogenate and in the upper one-third and lower two-thirds of isolated crypt units to be 74.9 ± 2.0, 59.8 ± 2.4, and 59.3 ± 3.2 fmol/mg protein, respectively, indicating the presence of aldosterone receptors in the crypt cell population. We conclude that in rat distal colon aldosterone-induced Na+ and K+ ...
Salimetrics has developed and validated an enzyme immunoassay for the measurement of the steroid hormone aldosterone in saliva. This assay is exclusively available via Salimetrics salivary testing.... (PRWeb October 04, 2012). Read the full story at http://www.prweb.com/releases/salivary_aldosterone/salimetrics/prweb9970342.htm ...
Sodium transport across the tight epithelia of Na+ reabsorbing tissues such as the distal part of the kidney nephron and colon is the major factor determining total-body Na+ levels, and thus, long-term blood pressure. Aldosterone plays a major role in sodium and potassium metabolism by binding to epithelial mineralocorticoid receptors (MR) in the renal collecting duct cells localized in the distal nephron, promoting sodium resorption and potassium excretion. Aldosterone enters a target cell and binds MR, which translocates into the nucleus and regulates gene transcription. Activation of MR leads to increased expression of Sgk-1, which phosphorylates Nedd4-2, an ubiquitin-ligase which targets ENAC to proteosomal degradation. Phosphorylated Nedd4-2 dissociates from ENAC, increasing its apical membrane abundance. Activation of MR also leads to increased expression of Na+/K+-ATPase, thus causing a net increase in sodium uptake from the renal filtrate. The specificity of MR for aldosterone is ...
Sodium transport across the tight epithelia of Na+ reabsorbing tissues such as the distal part of the kidney nephron and colon is the major factor determining total-body Na+ levels, and thus, long-term blood pressure. Aldosterone plays a major role in sodium and potassium metabolism by binding to epithelial mineralocorticoid receptors (MR) in the renal collecting duct cells localized in the distal nephron, promoting sodium resorption and potassium excretion. Aldosterone enters a target cell and binds MR, which translocates into the nucleus and regulates gene transcription. Activation of MR leads to increased expression of Sgk-1, which phosphorylates Nedd4-2, an ubiquitin-ligase which targets ENAC to proteosomal degradation. Phosphorylated Nedd4-2 dissociates from ENAC, increasing its apical membrane abundance. Activation of MR also leads to increased expression of Na+/K+-ATPase, thus causing a net increase in sodium uptake from the renal filtrate. The specificity of MR for aldosterone is ...
TY - JOUR. T1 - EFFECT OF ALDOSTERONE ON ANGIOTENSIN SKIN-TEST. AU - Spät, A.. AU - Sturcz, J.. AU - Purjesz, I.. PY - 1964/5/30. Y1 - 1964/5/30. UR - http://www.scopus.com/inward/record.url?scp=50549212861&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=50549212861&partnerID=8YFLogxK. U2 - 10.1016/S0140-6736(64)91240-1. DO - 10.1016/S0140-6736(64)91240-1. M3 - Letter. AN - SCOPUS:50549212861. VL - 283. SP - 1218. EP - 1219. JO - The Lancet. JF - The Lancet. SN - 0140-6736. IS - 7344. ER - ...
The localization of specific binding sites of four steroids--aldosterone, dexamethasone, 1-25-dihydroxycholecalciferol and estradiol--is described along the nephron. This localization has been determined by using an autoradiographic method on dry films, applied to intact microdissected tubular segments. Aldosterone binds specifically to nuclei of the distal and cortical collecting tubule. No specific labeling was observed in the cytoplasm. This localization corresponds to the known sites of action of aldosterone on sodium reabsorption. Specific nuclear binding of dexamethasone is present all along the tubule except the proximal tubule. In this latter part of the nephron, a specific cytoplasmic labeling is observed, in the absence of nuclear labeling. This cytoplasmic binding could correspond to physiological effects in this structure, via non-genomic mechanisms. 1-25(OH)2D3 nuclear binding is located mainly in the loop of Henle and medullary collecting tubule, which are the sites of synthesis of calcium
|strong|Sheep anti Aldosterone antibody|/strong| recognizes aldosterone, a steroid hormone (mineralocorticoid family) produced by the outer-section (zona glomerulosa) of the adrenal cortex in the adre…
Secreted by the adrenal cortex, aldosterone acts on the distal convoluted tube and causes reabsorption of sodium, potassium excretion ...
Case presentation A 20-year-old woman was being investigated privately for syncope in May 2017. Tilt-test showed that on standing, her heart rate increased by 30 beats/minute from baseline. She was referred to the cardiology team. Her body mass index (BMI) was 23 kg/m2 and average 24-hour ambulatory blood pressur ...
... is a hormone secreted by the adrenal glands outer cortex. Acting on the distal tubules and collecting ducts of the nephron, aldosterone stimulates the kidney to reabsorve sodium and release potassium, increasing blood pressure since sodium makes the body retain fluids. ...
Do not stop taking any medicine before talking to your doctor. Your provider may recommend that you eat no more than 3 grams of salt (sodium) per day for at least 2 weeks before the test. Or, your provider will recommend that you eat your usual amount of salt and also test the amount of sodium in your urine. At other times, the aldosterone blood test is done right before and after you receive a salt solution (saline) through the vein (IV) for 2 hours. Be aware that other factors can affect aldosterone measurements, including: ...
Its also called a serum aldosterone test. ALD is a hormone made by the adrenal glands. The adrenal glands are found on top of your kidneys and are responsible for producing several important hormones
The role of dopamine in the enhanced renal sensitivity to aldosterone (ALDO) seen in rats on a high potassium (high K+ ) diet Journal Articles ...
Hello, I just started using progesterone and Ive read that using amounts such as 100-2000 mg actually inhibits aldosterone and Im really scared because
Aldosterone answers are found in the Daviss Lab & Diagnostic Tests powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
Aldosterone, the mineral hormone Aldosterone is a mineral corticoid that is made in the part of the adrenal glands called the cortex. It is the major hormone controlling mineral and salt levels, especially sodium and potassium, and consequently, fluid balance within our bloodstream. It goes up when we are under stress. When it is high,…
Brussels, date At the Salt & Pregnancy Forum of May 2006 (1), organized by EuSalt, Prof. Dr. Markus G. Mohaupt already underlined that pregnancy is no time to reduce salt intake and that additional salt may benefit women suffering from pre-eclampsia.
Hi everyone I have been diagnosed with hashis and I also recently took an adrenal stimulation test and was diagnosed with adrenal fatigue. I am currently taking 2 grains of nature-throid and my doc j...
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. [PubChem]
GOAL: To describe the structure, synthesis, transport, metabolism and excretion of steroid hormones and the consequences of their deficiencies ...
Draw upright specimen after the patient is made to sit up for 30 min. Ship refrigerated or frozen. Overnight fasting is preferred ...
RESULTS Compared with baseline values, GFR (171 ± 20 to 120 ± 15 mL/min/1.73 m2) and filtration fraction (FF, 0.24 ± 0.06 to 0.18 ± 0.03) declined in hyperfilterers (ANOVA P ≤ 0.033), and renal vascular resistance increased (0.0678 ± 0.0135 to 0.0783 ± 0.0121 mmHg/L/min, P = 0.017). GFR and FF did not change in normofiltering subjects. In contrast, the radial augmentation index decreased in hyperfiltering (1.2 ± 11.7 to −11.0 ± 7.8%) and normofiltering (14.3 ± 14.0 to 2.5 ± 14.6%) subjects (within-group changes, ANOVA P ≤ 0.030). The decline in circulating aldosterone levels was similar in both groups. ...
This mechanism, which runs from renin through Ang II and to aldosterone, as well as the negative feedback that Ang II has on ... The renin-angiotensin-aldosterone system (RAAS) plays a key role in the pathology of cardiovascular disease, hypertension, ... Hsueh, W. A.; Wyne, K. (2011). "Renin-Angiotensin-Aldosterone System in Diabetes and Hypertension". The Journal of Clinical ... Ang II stimulates renal sodium retention; promotes aldosterone secretion; causes vasoconstriction, and increases sympathetic ...
Aldosterone synthase (CYP11B2) inhibitors such as metyrapone, mitotane, and osilodrostat prevent the production of the potent ... Jürg Müller (6 December 2012). Regulation of Aldosterone Biosynthesis. Springer Science & Business Media. pp. 39-. ISBN 978-3- ... and aldosterone from the less potent corticosteroids 11-deoxycorticosterone and 11-deoxycortisol and are used in the diagnosis ... mineralocorticoid aldosterone from the less potent mineralocorticoid corticosterone. Osilodrostat was investigated for the ...
HSD211B2 expression is also found in the brainstem in a small, aldosterone-sensitive subset of neurons located in the nucleus ... Corticosteroid 11-β-dehydrogenase isozyme 2 is an NAD+-dependent enzyme expressed in aldosterone-selective epithelial tissues ... This protective mechanism is necessary because cortisol circulates at 100-1000-fold higher concentrations than aldosterone, and ... "Aldosterone in the brain". American Journal of Physiology. Renal Physiology. 297 (3): F559-76. doi:10.1152/ajprenal.90399.2008 ...
Spironolactone, an aldosterone antagonist. This has two actions, firstly, as a potassium-sparing diuretic, although its ... Secondly, it reduces aldosterone-mediated myocardial fibrosis, possibly slowing the progression of heart disease. An ACE ...
Sodium absorption by the distal tubule is mediated by the hormone aldosterone. Aldosterone increases sodium reabsorption. ...
Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the ... Renin-angiotensin-aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water imbalance ... AI increases for the same reason; AII and aldosterone decrease. Bradykinin increases because of less inactivation by ACE. Under ... ACE inhibitors reduce the activity of the renin-angiotensin-aldosterone system (RAAS) as the primary etiologic (causal) event ...
Aldosterone receptor antagonists are not recommended as first-line agents for blood pressure,[35] but spironolactone and ... On the other hand, β-blockers, diuretics, ACE inhibitors, angiotensin receptor blockers, and aldosterone receptor antagonists ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
... associated with oxidative stress as well as inflammatory processes and an overactive renin-angiotensin-aldosterone system (RAAS ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
Aldosterone and cortisol levels are both reduced. Moderate 21-hydroxylase deficiency is referred to as simple virilizing CAH ... Cortisol is reduced, but aldosterone is not. Still milder forms of 21-hydroxylase deficiency are referred to as non-classical ... Neither aldosterone nor cortisol are reduced. The salt-wasting and simple virilizing types are sometimes grouped together as " ... Synthesis of aldosterone is also dependent on 21-hydroxylase activity. Although fetal production is impaired, it causes no ...
aldosterone. 52-39-1 C21H28O5. cortisone. 53-06-5 ...
aldosterone: Hyperaldosteronism/Primary aldosteronism *Conn syndrome. *Bartter syndrome. *Glucocorticoid remediable ...
Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the ... Stimulation by ATII of the adrenal cortex to release aldosterone, a hormone that acts on kidney tubules, causes sodium and ... Renin-angiotensin-aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water imbalance ... ATI increases for the same reason; ATII and aldosterone decrease. Bradykinin increases because of less inactivation by ACE. ...
Aldosterone, on the other hand, has differing levels. Levels are low in September to November, and rise to a maximum from ... In summer, aldosterone creates an increase in enzymatic activity (Lodi et al. 1995). Because of this increase in activity, ... 1995). Aldosterone, will independently cause an increase in Na+ channels within the cutaneous membrane. The ion transport is a ... In experiments allowing newts to be exposed to nonylphenol, there was a decrease in corticosterone and aldosterone. This is ...
Aldosterone has been found to have rapid non-genomic effects in the central nervous system, the kidneys, the cardiovascular ... It has been estimated that as much as 50% of the rapid actions of aldosterone are mediated by mMRs that are not the classical ... GPER, also known as GPR30, binds and is activated by aldosterone, and may be considered an mMR, although it also binds and is ... Harvey BJ, Alzamora R, Stubbs AK, Irnaten M, McEneaney V, Thomas W (2008). "Rapid responses to aldosterone in the kidney and ...
In rigid systems such as aldosterone, the 1,5-hydrogen atom transfer is exceedingly fast, with a rate constant on the order of ... Barton, D. H. R.; Beaton, J. M. (1960). "A Synthesis of Aldosterone Acetate". Journal of the American Chemical Society. 82 (10 ... a synthesis of aldosterone acetate is demonstrated. Allowing corticosterone acetate to react with nitrosyl chloride in dry ...
Renin-angiotensin-aldosterone system. http://edemainformation.blogspot.ca/2005/11/edema-pathophysiology-and-treatment.html ...
Aldosterone effects are mediated by the mineralocorticoid receptor (MR), a transcription factor highly expressed in the distal ... Osmotic Stress Regulates Mineralocorticoid Receptor Expression in a Novel Aldosterone-Sensitive Cortical Collecting Duct Cell ... which mediates aldosterone-stimulated Na+ reabsorption through the epithelial sodium channel activation. MR expression is ...
4) In a cell superfusion system, the aldosterone response to AII is biphasic. Suppressing the transient [Ca2+]i elevation ... Angiotensin II (AII) and K+ raise the cytosolic free Ca2+ concentration [(Ca2+]i) and stimulate aldosterone production in ... Quantitative analysis of the cytosolic-free-Ca2+-dependency of aldosterone production in bovine adrenal glomerulosa cells. ... Quantitative analysis of the cytosolic-free-Ca2+-dependency of aldosterone production in bovine adrenal glomerulosa cells. ...
It is used primarily to replace the missing hormone aldosterone in various forms of adrenal insufficiency such as Addisons ...
The defense against hyperkalemia: the roles of insulin and aldosterone. (opens in new tab) ...
... leading to hypersecretion of adrenal androgens with reduced production of cortisol and aldosterone), or aldosterone synthase ... primary defects in adrenal synthesis or secretion of aldosterone, and aldosterone resistance. The major clinical manifestations ... 1) Primary aldosterone deficiency should be suspected in persons who have hyperkalemia despite normal renal function and lack ... 3) Aldosterone resistance: Type I and type II pseudohypoaldosteronism, potassium-sparing diuretics that compete for the ...
Matsuoka, H., Mulrow, P.J., and Li, C. H., 1980, Beta-lipotropin: A new aldosterone-stimulating factor, Science 209: 307-308. ... Kern, D. C., Weinberger, M. H., Higgins, J. R., Kramer, N. J., Gomez-Sanchez, C., and Holland, O. B., 1978, Plasma aldosterone ... Plasma Renin Activity Congenital Adrenal Hyperplasia Primary Aldosteronism Plasma Aldosterone Zona Glomer These keywords were ... Kuchel, O., Buu, N. T., Vescei, P., Bourque, M., Harnet, P., and Genest, J., 1980, Are plasma aldosterone surges in primary ...
An aldosterone-producing adenoma is a noncancerous (benign) tumor that develops in an adrenal gland, which is a small hormone- ... Aldosterone-producing adenomas are caused by mutations in one of several genes. The most commonly mutated gene is KCNJ5, ... An aldosterone-producing adenoma is a noncancerous (benign) tumor that develops in an adrenal gland, which is a small hormone- ... In adrenal gland cells, this flow of ions helps control the production of aldosterone. Mutations in the KCNJ5, CACNA1D, or ...
This test measures the amount of aldosterone (ALD) in blood or urine. ALD is a hormone that helps control blood pressure and ... What is an aldosterone (ALD) test?. This test measures the amount of aldosterone (ALD) in your blood or urine. ALD is a hormone ... Why do I need an aldosterone test?. You may need this test if you have symptoms of too much or too little aldosterone (ALD). ... The combined tests are sometimes called an aldosterone-renin ratio test or aldosterone-plasma renin activity. ...
2010). Use of diurnal rhythm in salivary aldosterone to discriminate between bilateral adrenal hyperplasia and aldosterone ... Excess production of aldosterone is known to be involved in the development of hypertension, which is in turn associated with ... Aldosterone is an important steroid hormone that serves the crucial role of regulating sodium and potassium levels in the ... Receptors that bind aldosterone have also been identified for cell types other than those that regulate sodium and potassium ...
It selectively stimulates secretion of aldosterone. The secretion of aldosterone has a diurnal rhythm. Aldosterone is the ... Aldosterone is increased at low sodium intakes, but the rate of increase of plasma aldosterone as potassium rises in the serum ... Aldosterone is part of the renin-angiotensin-aldosterone system. It has a plasma half-life of under 20 minutes. Drugs that ... A measurement of aldosterone in blood may be termed a plasma aldosterone concentration (PAC), which may be compared to plasma ...
Aldosterone is synthesized by following the metabolism of progesterone. In the potential case where aldosterone synthase is not ... Deficient aldosterone synthase activity results in impaired biosynthesis of aldosterone while corticosterone in the zona ... Aldosterone synthase converts 11-deoxycorticosterone to corticosterone, to 18-hydroxycorticosterone, and finally to aldosterone ... Aldosterone synthase is encoded on chromosome 8q22 by the CYP11B2 gene. The gene contains 9 exons and spans roughly 7000 base ...
Aldosterone definition, a hormone produced by the cortex of the adrenal gland, instrumental in the regulation of sodium and ... aldosterone. First recorded in 1950-55; ald(ehyde) + -o- + ster(ol) + -one ... aldol, aldolase, aldomet, aldopentose, aldose, aldosterone, aldosteronism, aldoxime, aldrich, aldrich syndrome, aldrich, thomas ...
Molecules that are dissolved in water may dissociate into charged ions. An acid is a substance that increases the number of H+ ions in a solution. A base is a substance that decreases the number of H+ ions in a solution. The concentration of H+ ions in a solution can be measured and is called the pH of the solution.. The pH of a solution can be measured using a scale that ranges from 0 to 14. A solution of pH = 7 is neutral, a solution of pH lower than 7 is acidic, and a solution of pH greater than 7 is basic (alkaline). The number of H+ ions increases as the pH number decreases (and vice versa). The difference between two successive numbers on the pH scale represents a ten-fold difference in the H+ ion concentration because the scale is a logarithmic scale (log of base 10). For example, a solution with a pH of 2 has 10 times more H+ ions as a solution with a pH of 3. A solution with a pH of 2 has 100 times more H+ ions as a solution with a pH of 4. ...
Aldosterone is a steroid hormone of the mineralocorticoid family. It causes the kidneys to retain sodium and water. Get help ... See the latest posts about Aldosterone News & Opinion in womens health ... This Aldosterone News & Opinion page on EmpowHER Womens Health works best with javascript enabled in your browser.. Toggle ...
New aspects of rapid aldosterone signaling.. Grossmann C1, Gekle M.. Author information. 1. Julius-Bernstein-Institut für ... Aldosterone, the endogenous ligand of the mineralocorticoid receptor (MR) in humans, is a steroid hormone that regulates salt ... Altogether, the function of nongenomic aldosterone effects seems to be to modulate other signaling cascades, depending on the ... Besides genomic effects mediated by activated MR, rapid aldosterone actions that are independent of translation and ...
Control of aldosterone release from the adrenal cortexEdit. The renin-angiotensin system, showing role of aldosterone between ... Aldosterone is part of the renin-angiotensin-aldosterone system. It has a plasma half-life of under 20 minutes.[6] Drugs that ... A measurement of aldosterone in blood may be termed a plasma aldosterone concentration (PAC), which may be compared to plasma ... Aldosterone stimulates the secretion of K+ into the tubular lumen.[11]. *Aldosterone stimulates Na+ and water reabsorption from ...
Treatments and Tools for aldosterone. Find aldosterone information, treatments for aldosterone and aldosterone symptoms. ... aldosterone - MedHelps aldosterone Center for Information, Symptoms, Resources, ... I recently had my aldosterone and renin checked. The results were: Aldosterone 17.2, Renin ... ... High blood cortisol, high urine creatinine, high blood aldosterone - Family Health Expert Forum ...
aldosterone, serum 2 NG/DL *** After Stim Cortisol 27.6 MCG/DL 4.0-22.0 aldosterone, serum 3 NG/DL vitamin b12, serum 485 pg/mL ... aldosterone, serum 2 NG/DL *** After Stim Cortisol 27.6 MCG/DL 4.0-22.0 aldosterone, serum 3 NG/DL vitamin b12, serum 485 pg/mL ... Cortisol/Aldosterone levels help NicoleP1991 Hello Everyone, I appreciate you reading this question and taking the time to ... Cortisol/Aldosterone levels help. Hello Everyone, I appreciate you reading this question and taking the time to answer. I have ...
... and high aldosterone levels? I know that hypo-t can cause edema. Low corts and high aldosterone---is that due to being long- ... and high aldosterone levels? I know that hypo-t can cause edema. Low corts and high aldosterone---is that due to being long- ... yo-yo aldosterone levels. Hi, I was officially diagnosed with hypothyroid about 18 months ago but couldnt tolerate the natural ... I had very low aldosterone and very low cortisol levels (24-hour saliva test results from 6 1/2 months ago.) Of course I had ...
aldosterone Aldosterone is a hormone produced by the adrenal glands. It regulates the balance of salt and water in the body by ... Aldosterone also acts on the central nervous system to increase a persons appetite for salt and to make them thirsty. These ...
The Local Cardiac Renin-Angiotensin Aldosterone System, Second Edition updates new findings on the local renin-angiotensin ... Renin-Angiotensin-Aldosterone System and Cardiomyocyte Apoptosis in Hypertensive Heart Disease Arantxa González, Susana Ravassa ... Cardiac Effects of Aldosterone, the Bad, but Is There Also a Good? ... The Local Cardiac Renin-Angiotensin Aldosterone System, Second Edition updates new findings on the local renin-angiotensin ...
ALDOSTERONE. (11BETA)-11,21-DIHYDROXY-3,20-DIOXOPREGN-4-EN-18-AL. C21 H28 O5. PQSUYGKTWSAVDQ-ZVIOFETBSA-N. ... Taken together, these results explain the potency of MR activation by aldosterone, the weak activation induced by progesterone ...
Aldosterone-treated cells dramatically shrink when 1 μmol/L of the diuretic amiloride is applied. Cells deprived of aldosterone ... Human Endothelium: Target for Aldosterone. Hans Oberleithner, Thomas Ludwig, Christoph Riethmüller, Uta Hillebrand, Lars ... Aldosterone has long been known to control water and electrolyte balance by acting on mineralocorticoid receptors in kidney. ... Human Endothelium: Target for Aldosterone. Hans Oberleithner, Thomas Ludwig, Christoph Riethmüller, Uta Hillebrand, Lars ...
... , Selective Aldosterone Blocker, Aldosterone Antagonist, Eplerenone, Inspra. ... aldosterone inhibitor, ALDOSTERONE ANTAG, Aldosterone Antagonists, aldosterone inhibitors, aldosterone antagonists, aldosterone ... Aldosterone antagonists (product), Aldosterone antagonists (substance), Aldosterone antagonist (substance), Aldosterone ... Selective Aldosterone Receptor Antagonist. Selective Aldosterone Receptor Antagonist Aka: Selective Aldosterone Receptor ...
... with a raised log-transformed plasma aldosterone, although present AF at follow-up was related to a high aldosterone level (p ... Raised plasma aldosterone and natriuretic peptides in atrial fibrillation.. Dixen U1, Ravn L, Soeby-Rasmussen C, Paulsen AW, ... In this study, our aim was to evaluate at a long-term follow-up visit the levels of plasma aldosterone and natriuretic peptides ... Heart rhythm at follow-up visit (SR/AF), plasma aldosterone, plasma N-terminal pro Brain Natriuretic Peptide (Nt-proBNP), ...
  • The serum concentration of Afatinib can be decreased when it is combined with Aldosterone. (drugbank.ca)
  • 4) Circulating aldosterone, not bound to serum proteins, enters saliva by passive diffusion. (salimetrics.com)
  • Aldosterone (Pig) ELISA Kit is an immunoassay for the quantitative determination of aldosterone in Pig serum, plasma. (abnova.com)
  • Eplerenone binds to the mineralocorticoid receptor and blocks the binding of aldosterone, thereby decreasing sodium resorption and subsequently increasing water outflow. (fpnotebook.com)
  • Since the publication of 2 clinical trials, RALES (Randomized Aldactone Evaluation Study) and EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study), the role of aldosterone in cardiovascular remodeling has generated considerable attention. (ahajournals.org)
  • A newer class of drugs called selective aldosterone-receptor antagonists (SARAs) , such as eplerenone, block only aldosterone receptors, resulting in fewer side effects. (simstat.com)
  • A study called the Eplerenone Post-Acute Myo-cardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) tested the aldosterone blocker eplerenone in people with acute myocardial infarction (heart attack) complicated by left ventricular dysfunction and signs of heart failure who were receiving standard medical therapy. (diabetesselfmanagement.com)
  • We conducted a double-blind, placebo-controlled study evaluating the effect of eplerenone, a selective aldosterone blocker, on morbidity and mortality among patients with acute myocardial infarction complicated by left ventricular dysfunction and heart failure. (unboundmedicine.com)
  • Vascular inflammation was examined as a potential mechanism of aldosterone-mediated myocardial injury in uninephrectomized rats receiving 1% NaCl-0.3% KCl to drink for 1, 2, or 4 wk and 1 ) vehicle, 2 ) aldosterone infusion (0.75 μg/h), or 3 ) aldosterone infusion (0.75 μg/h) plus the selective aldosterone blocker eplerenone (100 mg · kg −1 · day −1 ). (physiology.org)
  • Because KCNJ5 mutated channels were reported to be specifically sensitive to inhibition by macrolide antibiotics, which concentration dependently blunts aldosterone production in HAC15 transfected with the G151R and L168R mutated channel, we herein tested the effect of clarithromycin on aldosterone synthesis and secretion in a pure population of aldosterone-secreting cells obtained by immunoseparation (CD56 + cells) from APA tissues with/without the 2 most common KCNJ5 mutations. (ahajournals.org)
  • First, aldosterone produced vascular injury in the presence of angiotensin-converting enzyme inhibition ( 25 ). (physiology.org)
  • Dietary sodium, aldosterone, and left ventricular mass changes during long-term inhibition of the renin-angiotensin system. (biomedsearch.com)
  • PI3K, p38 and ERK1/2 inhibition diminished these aldosterone-induced neutrophil productions. (sigmaaldrich.com)
  • The role of aldosterone and NADPH oxidases (Nox's) in the molecular mechanisms of age-associated vascular damage is unclear. (bmj.com)
  • There are two lines of evidence that suggest that the role of aldosterone in vascular injury is also independent of ANG II. (physiology.org)
  • Measure the amount of aldosterone released into the body by the adrenal glands. (parkviewmc.com)
  • The amount of aldosterone in blood changes depending on whether you are standing up or lying down. (nkch.org)
  • ACTH enters the circulation and signals the adrenal glands to release aldosterone, while at the same time signaling the release other adrenal steroid hormones. (prweb.com)
  • Aldosterone helps regulate the body's fluid levels and blood pressure by controlling the amount of salt retained by the kidneys. (medlineplus.gov)
  • Excess aldosterone causes the kidneys to retain more salt than normal, which increases the body's fluid levels and blood pressure. (medlineplus.gov)
  • Additionally, in recent years researchers have uncovered other "non-classical" effects of aldosterone within tissues in the heart, vascular system and kidneys, which lead to increased levels of inflammation and tissue damage. (prweb.com)
  • Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal GFR ( glomerular filtration rate ). (wikidoc.org)
  • However, RIA methods commonly used to measure aldosterone pose some analytical challenges, including long incubation times, the need to batch samples for cost-effectiveness, relatively short shelf life of radiolabeled reagents, and drawbacks related to the use of radioactive materials. (aacc.org)
  • Salimetrics' list of measurable biomarkers in saliva has expanded once again with the addition of an assay for salivary aldosterone. (prweb.com)
  • Salivary aldosterone has recently been confirmed to be a reliable alternative to plasma sampling, and ongoing studies are investigating the use of salivary aldosterone for the screening and diagnosis of diseases that affect circulating levels of this hormone. (prweb.com)
  • 9) Salivary aldosterone levels correspond approximately to 30% of those found in plasma, with good correlation found between plasma and non-extracted salivary aldosterone. (salimetrics.com)
  • 10) Salivary aldosterone levels are unaffected by salivary flow rate or hormone-binding proteins. (salimetrics.com)
  • A diurnal rhythm for salivary aldosterone exists for healthy individuals, with highest levels in the morning. (salimetrics.com)
  • As aldosterone has been implicated in the genesis of myocardial fibrosis, hypertrophy, and dysfunction, we sought to determine the effects of aldosterone antagonism on myocardial function in hypertensive patients with suspected diastolic heart failure by using sensitive quantitative echocardiographic techniques in a randomized, double-blinded, placebo-controlled study. (unboundmedicine.com)
  • Aldosterone antagonism improves myocardial function in hypertensive heart disease. (unboundmedicine.com)
  • Recent data ( 21 ) showing improved survival with the addition of aldosterone antagonism to standard therapy in patients with severe heart failure, independent of hemodynamic effects, support this hypothesis. (physiology.org)
  • Second, aldosterone antagonism results in marked vascular protection, even in the presence of ANG II infusions ( 24 ). (physiology.org)
  • These advances in our understanding of aldosterone physiopathology have shed light on the biological reasons which are at the base of the impressive results obtained in clinical trials of aldosterone antagonism. (eurekaselect.com)
  • D. Duval, J. W. Funder, The binding of tritiated aldosterone in the rat liver cytosol. (springer.com)
  • Other factors that physiologically regulate aldosterone release in concert with ATII and K + are corticotropin (ACTH, stimulatory) and atrial natriuretic peptide (ANP, inhibitory) ( 3 ). (frontiersin.org)
  • 1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. (clinsci.org)
  • p66SHC activation by aldosterone was blocked by ML171 (Nox1 inhibitor) in WKY and SHRSP VSMCs, and blunted in the vasculature from Nox1 knockout mice. (bmj.com)
  • Recent research has shown that excess aldosterone production can also be associated with obesity and the development of related diseases such as insulin resistance and diabetes. (prweb.com)
  • By proving the principle that the oversecretion of aldosterone can be specifically blunted in APA cells ex vivo with G151R and L168R mutations, these results provide compelling evidence of the possibility of specifically correcting aldosterone excess in patients with APA carrying the 2 most common KCNJ5 somatic mutations. (ahajournals.org)
  • Whether the improved left ventricular function observed in the Aldosterone Receptor Blockade in Diastolic Heart Failure trial is of clinical significance requires further investigation in larger populations," the authors write. (empr.com)
  • It is the sole enzyme capable of synthesizing aldosterone in humans and plays an important role in electrolyte balance and blood pressure. (wikipedia.org)
  • 1,2) Like the other steroid hormones that can be measured in saliva, aldosterone diffuses readily from the circulation into saliva where it can be conveniently measured without the pain and inconvenience of drawing blood samples. (prweb.com)
  • Your brain interprets these signals and sends messages to your adrenal glands, which then alter their release of hormones - epinephrine, norepinephrine and aldosterone - that control your heart rate, blood vessel diameter and kidney function. (livestrong.com)
  • Too much aldosterone can cause high blood pressure and a build-up of fluid in body tissues. (cancer.gov)
  • Aldosterone is a hormone that is released by the adrenal glands to aid your body in keeping your blood pressure regulated. (healthtestingcenters.com)
  • We have shown that mild, daily stress may be involved in the elevation of blood pressure (not only through the known catecholamine pathway) but also through the ACTH-aldosterone pathway," said lead author Athina Markou, MD, who is a Consultant Endocrinologist in the Department of Endocrinology and Diabetes Center, G. Gennimatas General Hospital, Athens, Greece. (endocrineweb.com)
  • However, whether aldosterone in the heart tissue is derived from the circulating blood or is produced locally, thereby contributing to remodeling, is unclear. (ahajournals.org)
  • Scientists have long known that aldosterone promotes the retention of sodium, which increases blood volume and thus raises blood pressure. (diabetesselfmanagement.com)
  • No specific binding protein for aldosterone has been identified in blood. (salimetrics.com)
  • An aldosterone test is often done at the time of a routine blood test. (nkch.org)
  • With maternal aldosterone deficiency in AS(-/-) mice, systolic blood pressure was low before and further reduced during pregnancy with no increase in proteinuria. (uzh.ch)