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.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.Databases, Chemical: Databases devoted to knowledge about specific chemicals.Databases, Pharmaceutical: Databases devoted to knowledge about PHARMACEUTICAL PRODUCTS.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Pharmacological Processes: The metabolism of drugs and their mechanisms of action.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)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.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.Water: A clear, odorless, tasteless liquid that is essential for most animal and plant life and is an excellent solvent for many substances. The chemical formula is hydrogen oxide (H2O). (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Adrenal Insufficiency: Conditions in which the production of adrenal CORTICOSTEROIDS falls below the requirement of the body. Adrenal insufficiency can be caused by defects in the ADRENAL GLANDS, the PITUITARY GLAND, or the HYPOTHALAMUS.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.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.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.Addison Disease: An adrenal disease characterized by the progressive destruction of the ADRENAL CORTEX, resulting in insufficient production of ALDOSTERONE and HYDROCORTISONE. Clinical symptoms include ANOREXIA; NAUSEA; WEIGHT LOSS; MUSCLE WEAKNESS; and HYPERPIGMENTATION of the SKIN due to increase in circulating levels of ACTH precursor hormone which stimulates MELANOCYTES.Adrenal Gland Diseases: Pathological processes of the ADRENAL GLANDS.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.Adrenal Gland Neoplasms: Tumors or cancer of the ADRENAL GLANDS.Cosyntropin: A synthetic peptide that is identical to the 24-amino acid segment at the N-terminal of ADRENOCORTICOTROPIC HORMONE. ACTH (1-24), a segment similar in all species, contains the biological activity that stimulates production of CORTICOSTEROIDS in the ADRENAL CORTEX.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).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.Thyroid Diseases: Pathological processes involving the THYROID GLAND.Hypothyroidism: A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA.Thyroid Gland: A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.Hyperthyroidism: Hypersecretion of THYROID HORMONES from the THYROID GLAND. Elevated levels of thyroid hormones increase BASAL METABOLIC RATE.Thyroid Function Tests: Blood tests used to evaluate the functioning of the thyroid gland.Thyroid Hormones: Natural hormones secreted by the THYROID GLAND, such as THYROXINE, and their synthetic analogs.Goiter: Enlargement of the THYROID GLAND that may increase from about 20 grams to hundreds of grams in human adults. Goiter is observed in individuals with normal thyroid function (euthyroidism), thyroid deficiency (HYPOTHYROIDISM), or hormone overproduction (HYPERTHYROIDISM). Goiter may be congenital or acquired, sporadic or endemic (GOITER, ENDEMIC).Thyroxine: The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.Thyroiditis, Autoimmune: Inflammatory disease of the THYROID GLAND due to autoimmune responses leading to lymphocytic infiltration of the gland. It is characterized by the presence of circulating thyroid antigen-specific T-CELLS and thyroid AUTOANTIBODIES. The clinical signs can range from HYPOTHYROIDISM to THYROTOXICOSIS depending on the type of autoimmune thyroiditis.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.Hyperaldosteronism: A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.Clarithromycin: A semisynthetic macrolide antibiotic derived from ERYTHROMYCIN that is active against a variety of microorganisms. It can inhibit PROTEIN SYNTHESIS in BACTERIA by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation.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.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.Adrenal Cortex Neoplasms: Tumors or cancers of the ADRENAL CORTEX.Potassium Channels, Inwardly Rectifying: Potassium channels where the flow of K+ ions into the cell is greater than the outward flow.Macrolides: A group of often glycosylated macrocyclic compounds formed by chain extension of multiple PROPIONATES cyclized into a large (typically 12, 14, or 16)-membered lactone. Macrolides belong to the POLYKETIDES class of natural products, and many members exhibit ANTIBIOTIC properties.Adenoma: A benign epithelial tumor with a glandular organization.Adrenal Gland Neoplasms: Tumors or cancer of the ADRENAL GLANDS.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.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.Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.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.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.Nephrons: The functional units of the kidney, consisting of the glomerulus and the attached tubule.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.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.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.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)Estradiol: The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids.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.Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.Corpus Luteum: The yellow body derived from the ruptured OVARIAN FOLLICLE after OVULATION. The process of corpus luteum formation, LUTEINIZATION, is regulated by LUTEINIZING HORMONE.Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.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)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.Heart Failure: A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.Canrenone: A synthetic pregnadiene compound with anti-aldosterone activity.Heart Failure, Systolic: Heart failure caused by abnormal myocardial contraction during SYSTOLE leading to defective cardiac emptying.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.Canrenoic Acid: A synthetic pregnadiene derivative with anti-aldosterone activity.Heart: The hollow, muscular organ that maintains the circulation of the blood.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.

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)

*Addison's disease

If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate. The frequency rate of ... Absent or insufficient levels of aldosterone stimulation of the renal distal tubule leads to sodium wasting in the urine and H+ ... In addition, many patients require fludrocortisone as replacement for the missing aldosterone. People with Addison's are often ... Hyperkalemia (raised blood potassium levels), due to loss of production of the hormone aldosterone. Eosinophilia and ...

*Hypoadrenocorticism in dogs

The adrenal glands secrete glucocorticoids such as cortisol and mineralocorticoids such as aldosterone; when proper amounts of ...

*Aldosterone

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 escape

In physiology, aldosterone escape is a term that has been used to refer to two distinct phenomena involving aldosterone that ... Aldosterone initially results in an increase in Na+ reabsorption in these patients through stimulation of ENaC channels in ... This is the proposed mechanism of "mineralocorticoid escape" for how patients with increased levels of aldosterone are able to ... The inability of ACE inhibitor therapy to reliably suppress aldosterone release, for example, in patients with heart failure or ...

*Aldosterone synthase

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-to-renin ratio

... can be given in ng/dL per ng/(mL·h), that is, nanogram per decilitre of aldosterone per nanogram per ... Aldosterone-to-renin ratio (ARR) is the mass concentration of aldosterone divided by the plasma renin activity in blood plasma ... Also, it can be given in pmol/liter per µg/(liter·h), where aldosterone is given in molar concentration. The former can be ... If the inverse ratio (i.e. renin-to-aldosterone) ratio is used, a value lower than the cutoff indicates primary ...

*Journal of the Renin-Angiotensin-Aldosterone System

... is a peer-reviewed academic journal that publishes papers in the field of ... Journal of the Renin-Angiotensin-Aldosterone System is abstracted and indexed in, among other databases: SCOPUS, and the Social ... Journal of the Renin-Angiotensin-Aldosterone System is a resource for biomedical professionals, including basic scientists and ... Journal of the Renin-Angiotensin-Aldosterone System also publishes research on other peptides, such as vasopressin, the ...

*Renin inhibitor

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 ...

*Steroidogenesis inhibitor

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 ...

*Corticosteroid 11-beta-dehydrogenase isozyme 2

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 ...

*Pimobendan

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 ...

*Distal convoluted tubule

Sodium absorption by the distal tubule is mediated by the hormone aldosterone. Aldosterone increases sodium reabsorption. ...

*ACE inhibitor

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 ...

*Italian crested newt

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 ...

*Membrane mineralocorticoid receptor

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 ...

*Barton reaction

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 ...

*Effective arterial blood volume

Renin-angiotensin-aldosterone system. http://edemainformation.blogspot.ca/2005/11/edema-pathophysiology-and-treatment.html ...

*Thiazide

This activates the renin-angiotensin system, stimulates the secretion of aldosterone, thus activating Na+/K+-ATPase, increasing ... J Renin Angiotensin Aldosterone Syst. 5 (4): 155-60. doi:10.3317/jraas.2004.034. PMID 15803433. Zhu Z, Zhu S, Liu D, Cao T, ... inhibition of sodium-chloride symporter at distal convoluted tubule of a nephron and stimulation of aldosterone that activates ...

*Cortisol

Bauman K, Muller J (1972). "Effect of potassium on the final status of aldosterone biosynthesis in the rat. I 18-hydroxylation ... The name cortisol is derived from cortex.) While the adrenal cortex also produces aldosterone (in the zona glomerulosa) and ... ISBN 0-471-06266-9. Muller AF, Oconnor CM (1958). An International Symposium on Aldosterone. Little Brown & Co. p. 58. Soffer ... Golf SW, Happel O, Graef V, Seim KE (November 1984). "Plasma aldosterone, cortisol and electrolyte concentrations in physical ...

*EMA401

J Renin Angiotensin Aldosterone Syst. 11 (1): 57-66. doi:10.1177/1470320309347790. US patent 4812462, BLANKLEY C JOHN; HODGES ... J Renin Angiotensin Aldosterone Syst. 11 (1): 57-66. doi:10.1177/1470320309347790. US patent 4812462, BLANKLEY C JOHN; HODGES ...

*Mineralocorticoid

Aldosterone is produced in the zona glomerulosa of the cortex of the adrenal gland and its secretion is mediated principally by ... Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as ... Aldosterone and cortisol (a glucosteroid) have similar affinity for the mineralocorticoid receptor; however, glucocorticoids ... Hypoaldosteronism (the syndrome caused by underproduction of aldosterone) leads to the salt-wasting state associated with ...

*Endothelin

Agapitov AV, Haynes WG; Haynes (March 2002). "Role of endothelin in cardiovascular disease". J Renin Angiotensin Aldosterone ...

*Adrenocortical hormone

For example, aldosterone functions to raise blood sodium levels and lower blood potassium levels by targeting the kidneys. ... Connell, J. M. C., & Davies, E. (2005). The new biology of aldosterone. Journal of Endocrinology, 186, 1-20.] Nelson, D. L., ... Examples of adrenocortical hormones that are involved in the stress response are aldosterone and cortisol. These hormones also ... hypoglycemia and decreased blood sodium levels and increased blood potassium levels caused by a deficiency of aldosterone. ...

*Hyperkalemia

... decreasing the activity of the renin-angiotensin-aldosterone system, and impairing tubular responsiveness to aldosterone Kim, ... There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone. In ... In chronic kidney disease, hyperkalemia occurs as a result of reduced aldosterone responsiveness and reduced sodium and watery ... Mineralocorticoid (aldosterone) deficiency or resistance can also cause hyperkalemia. Primary adrenal insufficiency are: ...

*Endocrine system

Colombo L, Dalla Valle L, Fiore C, Armanini D, Belvedere P (April 2006). "Aldosterone and the conquest of land". Journal of ... TRH - TSH - T3/T4 GnRH - LH/FSH - sex hormones CRH - ACTH - cortisol Renin - angiotensin - aldosterone leptin vs. insulin ... All vertebrates have some form of renin-angiotensin axis, and all tetrapods have aldosterone as primary mineralocorticoid. ...
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 ...
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 ...
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 ...
The key finding in this report is that Ang 1-7 can act as a negative modulator of aldosterone secretion in vitro and in vivo and can attenuate the aldosterone response to Ang II and ACTH, 2 of its classical secretagogues, acting directly on rat zona glomerulosa cells. Of note is also the observation that under our experimental conditions, Ang 1-7 did not affect potassium-induced aldosterone secretion. We cannot presently offer an explanation for the dichotomous inhibitory effect of Ang 1-7 in vitro, which is seemingly operative only in the setting of 2 different receptor-dependent secretory responses of aldosterone, mediated by angiotensin receptor type 1 (for Ang II) and the melanocortin receptor type 2 (for ACTH), but not in the presence of increasing concentrations of the direct membrane potential controlling K+. It is also noteworthy that Ang 1-7 lowered not only aldosterone but also Ang II-induced progesterone production, thus suggesting general interference with receptor-controlled ...
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. ...
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 Topeka. 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 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 Boca Raton. 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...
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. ...
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 ...
Principal objective:. To assess aldosterone resistance at birth by a non invasive measurement of urinary aldosterone, in order to evaluate its intensity as a function of gestational age. Determination of normal values of urinary aldosterone concentration in each group.. Secondary objectives:. Comparison of plasma and urinary electrolytes concentrations with hormonal measurements and clinical parameters. Evolution of these biological parameters throughout the first year of life, depending on gestational age at birth.. Methodology : multicentric study, open study Two hundred-forty newborns will be included in order to constitute 4 groups of 60 children, classified according to their gestational age: , 28 GW, 28 - , 33 GW, 33- , 37 GW, , 37 GW.. Inclusion criteria: every newborn will be included, after written parental consent was obtained.. Study :. Urinary samples will be collected onto a gauze compress, during the first 24 hours of life, at day three, and at 1, 3, 6 and 12 months. A blood sample ...
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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. ...
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.
The results of the present study demonstrate that plasma aldosterone levels are associated with plasma markers of insulin resistance and hyperinsulinemia in a white population of patients, the majority of whom had high blood pressure. Multivariate analysis demonstrates that this association is independent of plasma potassium and cortisol levels. In patients with hypertension, the relationship between aldosterone and decreased sensitivity to insulin was confirmed by direct assessment of insulin-mediated glucose disposal rates under a hyperinsulinemic-euglycemic clamp.. The issue of a possible relationship between plasma aldosterone and insulin resistance is important because aldosterone has been shown to contribute, independent of blood pressure, to the development of cardiovascular damage (8) and because insulin resistance and hyperinsulinemia are predictors of cardiovascular events in hypertensive patients (18), as in the general population (4). Initial demonstrations of an association between ...
Autori: Pojoga L, Gautier S, Blanc H, Guyene TT, Poirier O, Cambien F, Benetos A. Editorial: Am J Hypertens, 11, p.856-860, 1998.. Rezumat:. Cuvinte cheie: aldosterone, hypertension, genetics. ...
A deficiency in aldosterone can occur by itself or, more commonly, in conjunction with a glucocorticoid deficiency, and is known as hypoadrenocorticism or Addisons disease. Without treatment by mineralocorticoid replacement therapy, a lack of aldosterone is lethal, due to electrolyte imbalances and resulting hypotension and cardiac failure. Aldosterone excess is most commonly observed in two conditions: elevated plasma potassium (hyperkalemia) and low vascular volume. This should make sense considering that plasma potassium and angiotensin II are the major factors that regulate aldosterone secretion, as described above. Importantly, it is now recognized that roughly 1 in 10 cases of primary hypertension in humans is associated with hyperaldosteronism, due most commonly to aldosterone-secreting adrenal tumors or mutations in potassium channels.. ...
Home » Aldosterone. Aldosterone (Science: endocrinology, hormone) a steroid hormone produced by the adrenal cortex, that controls salt and water balance in the kidney. Abnormally high levels of this hormone cause sodium retention, high blood pressure, heart rhythum irregularities and possibly paralysis a corticosteroid hormone that is secreted by the cortex of the adrenal gland; regulates salt (sodium and potassium) and water balance.Aldosterone is a hormone that is involved in regulating sodium and potassium concentration in the body, and is excreted by the adrenal gland. It promotes the re-absorption of sodium back into the body and removes excess potassium. ...
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 ...
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 ...
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
... 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. ...
Aldosterone, in doses inappropriate to the salt status, plays an important role in the development of cardiovascular injury, including endothelial dysfunction, independent of its hypertensive effects. Acute non-genomic effects of aldosterone acting o
The role of dopamine in the enhanced renal sensitivity to aldosterone (ALDO) seen in rats on a high potassium (high K+ ) diet Journal Articles ...
A study presented at ACC.11, the American College of Cardiologys 60th Annual Scientific Session, revealed that administering a combination of aldosterone and angiotensin blockade for 4 months improves endothelial function compared with angiotensin blockade alone in women with signs and symptoms of ischemia and endothelial dysfunction.
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
ARAV : Collection Container/Tube: Preferred: Red top Acceptable: Serum gel Submission Container/Tube: Plastic vial Specimen Volume: 1.8 mL Additional Information: See Renin-Aldosterone Studies in Special Instructions for more detailed instructions.
According to Darwinian theory, complexity evolves by a stepwise process of elaboration and optimization under natural selection. Biological systems composed of tightly integrated parts seem to challenge this view, because it is not obvious how any elements function can be selected for unless the partners with which it interacts are already present. Here we demonstrate how an integrated molecular system-the specific functional interaction between the steroid hormone aldosterone and its partner the mineralocorticoid receptor-evolved by a stepwise Darwinian process. Using ancestral gene resurrection, we show that, long before the hormone evolved, the receptors affinity for aldosterone was present as a structural by-product of its partnership with chemically similar, more ancient ligands. Introducing two amino acid changes into the ancestral sequence recapitulates the evolution of present-day receptor specificity. Our results indicate that tight interactions can evolve by molecular ...
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]
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
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. ...
Angiotensin II (AII) and K+ raise the cytosolic free Ca2+ concentration [(Ca2+]i) and stimulate aldosterone production in isolated bovine adrenal glomerulosa cells. The mechanisms leading to an elevation of [Ca2+]i were analysed with the fluorescent Ca2+ probe quin 2. (1) Whereas [Ca2+]i rose transiently and returned to basal values within 5 min in response to AII, the effect of K+ was sustained for at least 15 min. (2) AII released Ca2+ from intracellular stores, whereas the [Ca2+]i response to K+ depended solely on extracellular [Ca2+]. (3) When added after K+ stimulation, AII provoked a dramatic decrease in [Ca2+]i to below the resting value. The role of [Ca2+]i in stimulating steroidogenesis was determined by manipulating the concentration of this cation. (4) In a cell superfusion system, the aldosterone response to AII is biphasic. Suppressing the transient [Ca2+]i elevation triggered by AII resulted in the disappearance of the initial secretory peak, but the final production rate was ...
Angiotensin II effects on cyclic AMP production and steroid output were studied in a sensitive preparation of isolated rat adrenal glomerulosa cells. With increasing concentrations of angiotensin II logarithmic dose-response curves for aldosterone and cyclic AMP production were similar. The minimum effective dose (0.2nm) for stimulation of aldosterone production also significantly (P,0.001) increased cyclic AMP output. For both aldosterone and cyclic AMP production, the peptide hormone concentration eliciting maximal response (0.2μm) and the ED50 (median effective dose) values (1nm) were the same; this is consistent with cyclic AMP acting as an intracellular mediator for angiotensin II-stimulated aldosterone production by glomerulosa cells. The angiotensin II antagonist [Sar1,Ala8]angiotensin II inhibited angiotensin II-stimulated corticosterone and aldosterone production in these cells. An equimolar concentration of antagonist halved the response to 20nm-angiotensin II, and complete inhibition ...
Historicallv, aldosterone was classified as a steroid hormone synthesized from the. I backbone cholesterol molecule in the. I mitochondria of the adrenal zona glomerulosa. Recent research has shown that it is produced in many extra-adrenal sites, including cardiovascular tissue. Since the adrenals contain only 1 to 2 pg aldosterone but secrete some 70 to 250 ,ig daily, yielding plasma levels of 5 to 100 pg/mL, it follows that their function is rapid aldosterone synthesis rather than storage. Over 85% of aldosterone is metabolized on first pass through the liver. Thus, its rate of degradation is dependent on hepatic blood flow and its extraction by parenchymal cells, each of which may be impaired in congestive heart failure (CHF).. The main stimuli to aldosterone synthesis by the zona glomerulosa cells are:. Angiotensin-II, the most potent stimulus, acts via AT-II type 1 (ATj) receptors; it also promotes growth of the zona glomerulosa.. Adrenocorticotrophic hormone (ACTH), a stress hormone: the ...
This is the first report of the effects of pharmacologic inhibition of aldosterone synthase in healthy human subjects. Results obtained with the ASI LCI699 indicate that the hormonal and renal effects of blocking the aldosterone pathway in healthy animals translate to humans. In healthy volunteers, once-daily oral dosing with LCI699 0.5 mg selectively reduced plasma and urinary aldosterone, which was associated with natriuresis and an increase in PRA. LCI699 prolonged survival in a rat disease model induced by ectopic overexpression of human renin and angiotensinogen, and was more effective than the MRA eplerenone in preventing cardiac and renal damage. These results support the therapeutic potential of inhibiting aldosterone synthase in diseases characterized by excessive aldosterone production.. Characterization of LCI699 was performed using in vitro assays and in vivo models in the rat and monkey. LCI699 showed distinct differences between species; it was at least 200-fold less potent in ...
BACKGROUND: Cosyntropin and metoclopramide can affect the subtyping of primary aldosteronism when used with adrenal vein sampling by exerting hormone- and side-specific effects on cortisol and aldosterone secretion. We investigated how these stimuli affect the selectivity index, the relative aldosterone secretion index, and the lateralization index in consecutive primary aldosteronism patients submitted to adrenal vein sampling. METHODS: We recruited 171 patients; of these, 149 underwent adrenal vein sampling before and after stimulation with cosyntropin (250 µg intravenous bolus, n= 53, 73% with an aldosterone-producing adenoma) or with metoclopramide (10 mg intravenous bolus, n= 96, 65% aldosterone-producing adenoma), and 32 with an aldosterone-producing adenoma were investigated for the relative gene expression of dopamine, melanocortin 2, and 5-hydroxytryptamine (serotonin) 4 receptor with microarrays ...
In the present study, the effects of hyperaldosteronism on myocardial injury in the setting of a high-salt diet were examined. There were three major findings of the present study. First, the data indicate that aldosterone/salt treatment induces leukocyte infiltration and injury of coronary arteries with associated ischemic and necrotic lesions of the adjacent myocardium. Second, we have identified the myocardial expression and progressive upregulation of the proinflammatory molecules osteopontin, MCP-1, and COX-2 in response to aldosterone/salt treatment. Third, the expression of proinflammatory molecules was diminished and vascular and cardiac pathology abrogated by treatment with the selective aldosterone blocker eplerenone, implicating a role for mineralocorticoid receptor stimulation in aldosterone/salt-induced myocardial injury. Although vascular inflammation seems to be the initial effect induced by aldosterone/salt treatment with the elevated myocardial expression of inflammatory ...
Hyperaldosteronism, also aldosteronism, is a medical condition wherein too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of potassium in the blood (hypokalemia) and increased hydrogen ion excretion (alkalosis). This cause of mineralocorticoid excess is primary hyperaldosteronism reflecting excess production of aldosterone by adrenal zona glomerulosa. Bilateral micronodular hyperplasia is more common than unilateral adrenal adenoma. Play media It can be asymptomatic, but these symptoms may be present: Fatigue Headache High blood pressure Hypokalemia Hypernatraemia Hypomagnesemia Intermittent or temporary paralysis Muscle spasms Muscle weakness Numbness Polyuria Polydipsia Tingling Metabolic alkalosis The causes of primary hyperaldosteronism are adrenal hyperplasia and adrenal adenoma (Conns syndrome). These cause hyperplasia of aldosterone-producing cells of the adrenal cortex resulting in primary hyperaldosteronism. The causes of secondary ...
TY - JOUR. T1 - Aldosterone-induced oxidative stress and inflammation in the brain are mediated by the endothelial cell mineralocorticoid receptor. AU - Dinh, Quynh N. AU - Young, Morag J. AU - Evans, Megan A. AU - Drummond, Grant R. AU - Sobey, Christopher G. AU - Chrissobolis, Sophocles. PY - 2016. Y1 - 2016. N2 - Elevated aldosterone levels, which promote cerebral vascular oxidative stress, inflammation, and endothelial dysfunction, may increase stroke risk, independent of blood pressure and other risk factors. The main target receptor of aldosterone, the mineralocorticoid receptor (MR), is expressed in many cell types, including endothelial cells. Endothelial cell dysfunction is thought to be an initiating step contributing to cardiovascular disease and stroke; however the importance of MR expressed on endothelial cells in the brain is unknown. Here we have examined whether endothelial cell MR mediates cerebral vascular oxidative stress and brain inflammation during aldosterone excess. In ...
Aldosterone mineralocorticoid hormone, produced by the adrenal gland. Atoms are represented as spheres with conventional colour coding: hydrogen (white), carbon (black), oxygen (red). - Stock Image F011/3801
Somatotropin treatment in chronically hypophysectomized, sodium-deprived rats effectively restored to treated animals the distinct and enhanced aldosterone secretory responsiveness of the adrenal which characterizes the adrenals of intact rats subjected to dietary sodium restriction, but absent in chronic and nontreated, adenohypophysectomized or totally hypophysectomized rats subjected to similar conditions of ... read more dietary sodium restriction. Treatment with β1−24ACTH(Zn) alone was ineffective, albeit adrenal weight and glucocorticoid secretory responsiveness were effectively maintained. The observed efficacious effect of somatotropin is similar and indistinguishable from the previously demonstrated effect produced by treatment of anterior pituitary powder in chronically hypophysectomized, sodium-deprived rats. The earlier findings that somatotropin is without any direct or specific stimulatory effect on aldosterone secretion and that treatment of intact, sodium-repleted rats with ...
Hyperaldosteronism is a medical condition where too much aldosterone is produced by the adrenal glands , which can lead to lowered levels of potassium . In hyperaldosteronism, overproduction of aldosterone leads to fluid retention and increased blood pressure, weakness, and, rarely, periods of paralysis. Aldosterone production is regulated partly by corticotropin (secreted by the pituitary gland) and partly through the renin-angiotensin-aldosterone system. Renin, an enzyme produced in the kidneys, controls the activation of the hormone angiotensin, which stimulates the adrenal glands to produce aldosterone. Hyperaldosteronism can be caused by a tumor (usually a noncancerous adenoma) in the adrenal gland (a condition called Conns syndrome), although sometimes both glands are involved and are overactive. Sometimes hyperaldosteronism is a response to certain diseases, such as very high blood pressure (hypertension) or narrowing of one of the arteries to the kidneys. Other causes of ...
The present study demonstrates that in the TG (mREN2)27 rat model, local adrenal renin, and not circulating renin of renal origin, plays a pivotal role in the regulation of mineralocorticoid biosynthesis and secretion in response to salt restriction. The major finding of the present study is that the adrenal renin-angiotensin system regulates mineralocorticoid production through the AT1-angiotensin II receptor subtype. Our experiments also show that the mouse transgene and not the endogenous renin is involved in the regulation of aldosterone biosynthesis in the adrenals of TG rats.. The hypertensive rat strain TG (mREN2)27 is transgenic for murine Ren-2d gene, providing an excellent tool for the investigation of the function of renin-angiotensin systems in specific tissues. The transgene, in fact, is overexpressed particularly in extrarenal tissues, such as in the zona glomerulosa and fasciculata of the adrenal cortex.4 Since plasma steroid levels and urinary steroid concentrations markedly ...
The regulation of aldosterone synthesis by the adrenal zona glomerulosa (ZG) cell involves a complex interaction between a wide variety of endogenous stimulatory and inhibitory factors. Angiotensin II (AII), adrenocorticotropic hormone, and potassium ion are the primary secretagogues stimulating aldosterone synthesis (Quinn and Williams, 1988). Atrial natriuretic peptide and decreasing oxygen concentration have been identified as inhibitory factors (Campbell et al., 1985; Raff et al., 1989). Recent investigations in a number of laboratories have indicated the inhibitory effects of NO on the synthesis of various steroid hormones (Adams et al., 1992; Natarajan et al., 1997; Cymeryng et al., 1998). The mechanism of NO inhibition of aldosterone synthesis involves a direct interaction with the cytochrome P450 enzymes required for the multistep conversion of cholesterol into aldosterone (Hanke et al., 1998). The inhibitory effects of NO and the ability of nitric oxide to bind to the cytochrome P450 ...
Eight normal male subjects were placed on a constant 10 mEq sodium, 60 mEq potassium diet for 5 days. At 8:00 a.m. on the 5th day, the subjects were given a standard dose of 100 mEq of sodium orally or intravenously. Subjects receiving oral sodium also received 200ml of 5% dextrose in water intravenously, and those receiving intravenous sodium also received placebo capsules orally. Water intake and posture were controlled. The subjects then returned to a free diet for 1 month and subsequently were restudied by using the opposite route of sodium administration. The subjects given the oral sodium load excreted greater quantities of sodium in their urine than those repleted intravenously. The differential natriuresis was significant as early as 2 hours after sodium loading. Plasma aldosterone concentration was similar irrespective of the route of sodium administration. Six patients with primary adrenocortical insufficiency and documented hypoaldosteronism were studied with the same protocol after 5 ...
Background--Aldosterone may have adverse effects in the myocardium and vasculature. Treatment with an aldosterone antagonist reduces cardiovascular risk in patients with acute myocardial infarction complicated by heart failure (HF) and left ventricular systolic dysfunction. However, most patients with acute coronary syndrome do not have advanced HF. Among such patients, it is unknown whether aldosterone predicts cardiovascular risk. Methods and Results--To address this question, we examined data from the dal-OUTCOMES trial that compared the cholesteryl ester transfer protein inhibitor dalcetrapib with placebo, beginning 4 to 12 weeks after an index acute coronary syndrome. Patients with New York Heart Association class II (with LVEF
At the meeting of The American College of Physicians in Los Angeles in 1956 we reported our preliminary findings of a significantly greater urinary aldosterone excretion in patients with severe essential and malignant hypertension than in normal subjects. This study was based on a biological determination of a purified aldosterone fraction obtained after two successive chromatographic purifications of the crude, neutral extract of acidified urine (1). These studies of the relationship of adrenocortical hormones to hypertensive disease have been continued and, by using a more specific physicochemical method for the isolation and determination of urinary aldosterone, have been extended to ...
Many medicines may change the results of this test. Be sure to tell your doctor about all the nonprescription and prescription medicines you take. You may be asked to stop taking some medicines for 2 weeks before the test. These include hormones (such as progesterone and estrogens), corticosteroids, diuretics, and many medicines used to treat high blood pressure, especially spironolactone (Aldactone), eplerenone (Inspra), and beta-blockers.. The amount of aldosterone in blood changes depending on whether you are standing up or lying down. If initial results show a problem, repeat tests may be done in different positions and under different conditions, such as not eating before the test or eating foods that contain a specific amount of salt. Your doctor may ask you to have your blood drawn at a certain time because aldosterone levels are highest in the early morning.. Talk to your doctor about any concerns you have regarding the need for the test, its risks, how it will be done, or what the ...
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It is well known that primary aldosteronism (PA) is the most common form of secondary hypertension, and also that aldosterone-producing adenoma and bilateral are the most common forms of PA.
... , also known as Conns syndrome, is considered one of the most common causes of secondary hypertension or high blood pressure. Primary aldosteronism occurs when your body produces too much aldosterone, which is a hormone that controls the sodium and patassium levels in the blood. When too much aldosterone is produced, the result is too much salt (sodium) and too little potassium in the blood, which leads to hypertension. Conns syndrome is more common in females than males and can occur at any age, but most commonly in people in their 30s and 40s. Symptoms may include muscle weakness, frequent urination, excessive thirst, or muscle twitching and cramps. Medical therapy is a good treatment option ...
BACKGROUND: Cosyntropin and metoclopramide can affect the subtyping of primary aldosteronism when used with adrenal vein sampling by exerting hormone- and side-specific effects on cortisol and aldosterone secretion. We investigated how these stimuli affect the selectivity index, the relative aldosterone secretion index, and the lateralization index in consecutive primary aldosteronism patients submitted to adrenal vein sampling. METHODS: We recruited 171 patients; of these, 149 underwent adrenal vein sampling before and after stimulation with cosyntropin (250 µg intravenous bolus, n= 53, 73% with an aldosterone-producing adenoma) or with metoclopramide (10 mg intravenous bolus, n= 96, 65% aldosterone-producing adenoma), and 32 with an aldosterone-producing adenoma were investigated for the relative gene expression of dopamine, melanocortin 2, and 5-hydroxytryptamine (serotonin) 4 receptor with microarrays ...
A formal metabolic study of carbenoxolone sodium (Biogastrone) 300 mg./day has been performed for 17 days on a woman with gastric ulcer who in a previous 21-day trial, on a 52-mEq sodium diet, showed weight gain, retention, and rise in plasma sodium and chloride concentrations, as well as hypokalaemia without change in potassium balance. In the present trial sodium intake was restricted to 26 mEq/day; while plasma electrolyte changes of lesser degree still occurred, there was no retention of water, sodium, or chloride. Aldosterone secretion in the control period was 202 μg./24 hours, and fell to 74 μg./24 hours after carbenoxolone, but plasma renin was unchanged.. These results suggest that the mineralocorticoid effects of carbenoxolone (and presumably of liquorice and its other derivatives) are due to an intrinsic aldosterone-like action, and that, with sodium deprivation, aldosterone secretion is suppressed by a mechanism which is not renin-mediated-possibly hypokalaemia.. ...
View Notes - Ch. 44 study guide from BIOL 50755 at University of Texas-Tyler. apparatus, angiotensin II, aldosterone, renin, atrial natriuretic factor. Knowledge goals: List an example of an
Activation of the mineralocorticoid receptor (MR) is implicated in clinical hypertension and target organ damage even in patients who have normal or low plasma...
Acting on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and the collecting duct of the kidney nephron, it increases the permeability of the apical (luminal) membrane to potassium and sodium and activates the basolateral Na+/K+ pumps, stimulating ATP hydrolysis leading to phosphorylation of the pump and a conformational change in the pump exposes the Na+ ions to the outside. The phosphorylated form of the pump has a low affinity for Na+ ions, hence reabsorbing sodium (Na+) ions and water into the blood, and secreting potassium (K+) ions into the urine. (Chlorine anions are also reabsorbed in conjunction with sodium cations to maintain the systems electrochemical balance ...
Helpful, trusted answers from doctors: Dr. Schwartz on aldosterone plasma renin act ratio: Sodium regulation is complex and not directly related to any single hormone. Mineralocorticoids like Fludrocortisone can increase sodium a bit and do cause sodium retention of sodium, but the sodium level is mostly regulated by a hormone called adh (vasopressin).
But sympathetic activity was not increased in the females. That begged the question: What was driving their hypertension? What we observed is that their aldosterone level was sky high, says Belin de Chantemele. While aldosterone also has a positive role in regulating blood pressure, high levels of the steroid hormone are associated with many things that are bad for the cardiovascular system like inflammation and blood vessel stiffness and scarring.. They took a step back and examined the enzyme producing aldosterone, CYP11B2, and found it was also very high in the females. As they began to put the pieces together, they realized that it was leptin that was a direct regulator of the increased aldosterone production by the adrenal gland in the female mice. Since both genders of these mice were hypersensitive to leptin, they were hypertensive but not fat. So they decided to also look at the connection in obese mice, which clearly make more leptin. In the face of high leptin levels, and as with ...
Context:Although confirmatory testing to verify aldosterone excess is a key step in the diagnosis of primary aldosteronism (PA), there is no consensus as to whether it is always needed and which of the tests need to be performed.Objective:The objecti
This study was conducted to assess the relationship between aldosterone synthase CYP1A1 MspI gene polymorphism and prostate cancer risk using meta-analysis.The search was conducted in PubMed and China Biological Medicine Database disc on October 1, 2015, and eligible reports were recruited and synthesized using meta-analysis method.
A continuous line of cells (A6) derived from toad kidney has been shown to form epithelia in culture that manifest aldosterone-stimulatable transepithelial sodium transport. In this study an efficient filtration assay for nuclear binding of [3H]aldosterone was validated. Specific high-affinity aldosterone and corticosterone binding sites in the particulate (nuclear-enriched) fraction were characterized in intact epithelia. Despite metabolism of both steroids, two high-affinity binding sites for each were demonstrable: aldosterone, Kd1 = 0.85 (+/- 0.19) X 10(-10) and Kd2 = 1.6 (+/- 0.42) X 10(-8) M; corticosterone, Kd1 = 0.5 (+/- 0.31) X 10(-10) and Kd2 = 0.32 (+/- 0.19) X 10(-8) M. Analogue competition-binding studies indicated a qualitative difference in the two sites and co-occupancy of both sites by the two steroids. The sodium transport response to aldosterone and corticosterone approximated a linear function of occupancy of the lower affinity sites. Although the lower affinity sites ...
In hypertension, the vasculature undergoes premature ageing. The role of aldosterone and NADPH oxidases (Noxs) in the molecular mechanisms of age-associated vascular damage is unclear. We hypothesise that premature ageing in hypertension is due to increased aldosterone-induced Nox activation. We assessed vascular ageing in resistance arteries and vascular smooth muscle cells (VSMCs) from adult WKY (18 weeks), aged WKY (52 weeks) and adult stroke-prone spontaneously hypertensive (SHRSP) rats. Blood pressure (BP) was measured by tail-cuff. Vascular structure and function were analysed by pressure and wire myography. Gene and protein expression were assessed by qPCR and immunoblotting. We observed elevated BP, endothelial dysfunction and hypercontractility in vessels from SHRSP (vs. WKY). Vascular contraction in aged WKY rats was similar to SHRSP rats. Increased stiffness was observed in mesenteric arteries from aged WKY and SHRSP rats (vs. WKY). Nox2, NoxA1 and NoxO1 mRNA expression was increased ...
Did you know that you could prevent or improve heart disease with just two teaspoons of our apple cider vinegar a day? Thats cheaper than any medication available on the market! But you dont just have to take our word for it. This fact has been proven by medical science over and over again.. One study showed that vinegar or acetic acid solution mixed with a normal diet in rats reduced their systolic blood pressure (thats the top number on the blood pressure reading) by up to 20mmHg! Vinegar lowered the activity of renin and aldosterone by up to 40% and 25% respectively. Renin and aldosterone are two hormones in the body that work to increase blood pressure. So, lowering their activity would enable better control of the disease.. Translating this to a human trial, a lower risk of fatal heart disease was reported in the Nurses Health Study, a study that involved thousands of people. This particular benefit was seen in nurses who consumed salads topped with oil and vinegar dressings regularly. ...
Spironolactone works by blocking the actions of a hormone in the body called aldosterone. This hormone is produced by glands found above the kidneys called the adrenal glands.. Aldosterone acts in the kidneys, where it is involved in controlling the balance of salt and water in the body. ...
Spironolactone works by blocking the actions of a hormone in the body called aldosterone. This hormone is produced by glands found above the kidneys called the adrenal glands.. Aldosterone acts in the kidneys, where it is involved in controlling the balance of salt and water in the body. ...
Micronized, time-release pregnenolone (plant source) in a lipidmatrix. Superior delivery form. In the body, pregnenolone ismetabolized from cholesterol by the cytochrome P450 enzyme.It serves as a parent hormone for all adrenal cortical steroids,including progesterone, testosterone, dehydroepiandrosterone,dihydrotestosterone, aldosterone, cortisol and estradiol.Pregnenolone levels decrease with age, during periods offatigue, or in conditions of inadequate cholesterol production.Suggested use:As a dietary supplement, 1 tablet daily with a meal, or as directedby a healthcare practitioner.CAUTION: This product is a hormone, influencing the productionof other hormones. Regular hormone testing is recommended.Cancer patients should consult their healthcare practitionerbefore use.
Tomashefsky, C. Steven, "Cumulative effects of aldosterone administration on three inbred strains of mice." (1967). Summer and Academic Year Student Reports. 1504 ...
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Although initially considered a rarity, primary aldosteronism now is considered one of the more common causes of secondary hypertension (HTN). Litynski reported the first cases, but Conn was the first to well characterize the disorder, in 1956.
View Notes - Ch52 salt and water balance and nitrogen excretionVRE from LS 2 at UCLA. Figure 52.15 Renin-Angiotensin-Aldosterone System Helps Regulate GFR Figure 52.15 Renin-Angiotensin-Aldosterone
Pseudohypoaldosteronism 1, autosomal dominant (PHA1A) [MIM:177735]: A salt wasting disease resulting from target organ unresponsiveness to mineralocorticoids. PHA1A is a mild form characterized by target organ defects confined to kidney. Patients may present with neonatal renal salt wasting with hyperkalaemic acidosis despite high aldosterone levels. These patients improve with age and usually become asymptomatic without treatment. {ECO:0000269,PubMed:11134129, ECO:0000269,PubMed:12788847, ECO:0000269,PubMed:16954160, ECO:0000269,PubMed:16972228}. Note=The disease is caused by mutations affecting the gene represented in this entry ...
We have previously reported that Dot1a is located in the cytoplasm and nucleus, widely expressed in kidney as detected by its histone H3 K79 methyltransferase activity, and involved in transcriptional control of the epithelial Na+ channel subunit α gene (αENaC). Aldosterone releases repression of αENaC by reducing expression of Dot1a and its partner AF9 and by impairing Dot1a-AF9 interaction via Sgk1-mediated AF9 phosphorylation. This network also appears to regulate transcription of several other aldosterone target genes. Here we provide evidence showing that Dot1a contains at least three potential nuclear localization signals (NLS). Deletion of these NLSs causes GFP-fused Dot1a fusions to localize almost exclusively in the cytoplasm of 293T cells as revealed by confocal microscopy. Deletion of NLSs abolished Dot1a-mediated repression of αENaC-promoter luciferase construct in M1 cells. AF9 is widely expressed in mouse kidney. Similar to αENaC, the mRNA levels of βENaC, γENaC, and Sgk1 ...
Receptor for prostaglandin E2 (PGE2). The activity of this receptor is mediated by G(s) proteins that stimulate adenylate cyclase. Has a relaxing effect on smooth muscle. May play an important role in regulating renal hemodynamics, intestinal epithelial transport, adrenal aldosterone secretion, and uterine function.
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D-ALDOSTERONE 21-ACETATE/ACM297916 can be provided in Alfa Chemistry. We are dedicated to provide our customers the best products and services.
Another name for Aldosteronism is Aldosteronism. Treatment for aldosteronism depends on the underlying cause, but the goal is to reduce high blood pressure ...
Another name for Aldosteronism is Aldosteronism. The following are some important questions to ask before and after the treatment of aldosteronism. Questions ...
For jimmylegs...re: zinc (btw, thanks for the recommendation. It *does* make some things more erm...climatic. ) http://www.ncbi.nlm.nih.gov/pubmed/17616752 Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2361-6. Epub 2007 Jul 6. Zinc dyshomeostasis in rats with aldosteronism. Response to spironolactone. Thomas M, ...
Guarda il video: Testing Vitamin D beyond 25-OHGuarda il video: Use of the Aldosterone and Renin Ratio for earlier diagnosis of Primary Aldosteronism
The suprarenal glands produce a variety of hormones. The adrenal marrow produces two hormones, the adrenaline and noradrenaline, also well-known as epinephrine and norepinephrine. These hormones are important in the regulation of many functions in the organism, including the heart frequency and blood pressure. The adrenal cortex produces three important hormones: the aldosterone, the cortisol and the Dehiepiandrosterone. The aldosterone regulates the kidneys salt and water absorption, as well as the blood pressure. The cortisol acts to regulate a series of corporal functions, including the metabolism of the glucose, the metabolism of the proteins, the growth of the bone, the blood pressure and the activity of the immune system ...
Clin Endocrinol (Oxf). 2010 Mar;72(3):305-11. doi: 10.1111/j.1365-2265.2009.03631.x. Epub 2009 May 16.. High prevalence of autonomous cortisol and aldosterone secretion from adrenal adenomas.. Piaditis GP, Kaltsas GA, Androulakis II, Gouli A, Makras P, Papadogias D, Dimitriou K, Ragkou D, Markou A, Vamvakidis K, Zografos G, Chrousos G ...
Aldosterone antagonists (or aldosterone blockers) are a class of medications used to treat high blood pressure and heart failure. They work on the same hormone system as ACE inhibitors and ARBs, but in a slightly different way. Aldosterone antagonists block the receptors in the body for the hormone aldosterone, causing the kidneys to hold onto more potassium and get rid of more fluid by increasing urine output. Less fluid in the body means lower blood pressure and less total blood volume, reducing the hearts workload and easing the strain on the heart. Getting rid of excess fluid helps relieve the symptoms of heart failure that are caused by fluid buildup, such as shortness of breath and swelling in the legs.. Aldosterone antagonists are not routine therapy for women with heart failure because they are less proven than other medications in the same class, including ACE inhibitors and ARBs. but are beneficial in selected women with systolic heart failure(blood pumping problems) who have recently ...
Effects of mineralocorticoid receptor antagonists in patients with hypertension and diabetes mellitus: A systematic review and meta-analysisEffects of mineralocorticoid receptor antagonists in patients with hypertension and diabetes mellitus: A systematic review and meta-analysisAA10730093 ...
definition of APA, what does APA mean?, meaning of APA, Aldosterone-Producing Adenoma, APA stands for Aldosterone-Producing Adenoma
In medicine (endocrinology), hypoaldosteronism refers to decreased levels of the hormone aldosterone. Isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol. (The two hormones are both produced by the adrenals.) There are several causes for this condition, including adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors). Primary Aldosterone deficiency Primary adrenal insufficiency Congenital adrenal hyperplasia (21 and 11β but not 17) Aldosterone synthase deficiency Secondary Aldosterone deficiency Secondary adrenal insufficiency Diseases of the pituitary or hypothalamus Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction) Renal dysfunction-most commonly diabetic nephropathy NSAIDs Ciclosporin Aldosterone deficiency should be treated with a mineralocorticoid (such as fludrocortisone), as well as possibly a ...
Our immunohistochemistry results indicated that the MR was not primarily located in the nucleus in normal DRG, translocating there only early after DRG inflammation. For the classical nuclear actions of the MR receptor, such translocation is generally taken as evidence for activation. The observations in normal DRG may seem to contradict the general view that the MR in most tissues should be chronically activated by basal plasma levels of corticosterone (except in tissues such as kidney where corticosterone is enzymatically degraded)-the affinity of the MR for corticosterone is higher than its affinity for aldosterone, so the (much higher) basal plasma levels of corticosterone should chronically activate the MR. RNA for the enzyme that degrades corticosterone in classical aldosterone-sensitive tissues, 11-hydroxysteroid dehydrogenase type II, is present in DRG21 though it is not known if this is neuronal or perhaps associated with vascular cells. In addition, the MR can apparently have forms ...
Glucocorticoid-induced leucine zipper (GILZ) is a mediator of the anti-inflammatory activities of glucocorticoids. However, GILZ deletion does not impair the anti-inflammatory activities of exogenous glucocorticoids in mice arthritis models and GILZ could also mediate some glucocorticoid-related adverse events. Osteoarthritis (OA) is a metabolic disorder that is partly attributed to adipokines such as leptin, and we previously observed that glucocorticoids induced leptin secretion in OA synovial fibroblasts. The purpose of this study was to position GILZ in OA through its involvement in the anti-inflammatory activities of glucocorticoids and/or in the metabolic pathway of leptin induction. The influences of mineralocorticoids on GILZ and leptin expression were also investigated. Human synovial fibroblasts were isolated from OA patients during knee replacement surgery. Then, the cells were treated with a glucocorticoid (prednisolone), a mineralocorticoid (aldosterone), a glucocorticoid receptor (GR)
Approach and Results-We report that administration of deoxycorticosterone acetate (DOCA) and salt or aldosterone and salt, but not DOCA or salt alone, to C57BL/6 male mice induced abdominal and thoracic aortic aneurysm formation and rupture in an age-dependent manner. DOCA and salt- or aldosterone and salt-induced aortic aneurysm mimicked human aortic aneurysm with respect to elastin degradation, inflammatory cell infiltration, smooth muscle cell degeneration and apoptosis, and oxidative stress. Aortic aneurysm formation did not correlate with the increase in blood pressure induced by DOCA and salt. Systemic administration of the angiotensin-converting enzyme inhibitor, enalapril, or angiotensin type 1 receptor antagonist, losartan, did not affect DOCA and salt-induced aortic aneurysm. In contrast, the mineralocorticoid receptor antagonists, spironolactone or eplerenone, significantly attenuated DOCA and salt- or aldosterone and salt-induced aortic aneurysm.. ...
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Addisons diseaseAddison's disease

Aldosterone. Aldosterone belongs to a class of hormones called mineralocorticoids, also produced by the adrenal glands. It ... Because patients with secondary adrenal insufficiency normally maintain aldosterone production, they do not require aldosterone ... When aldosterone production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume ... If aldosterone is also deficient, it is replaced with oral doses of a mineralocorticoid called fludrocortisone acetate ( ...
more infohttp://ringlingdocents.org/addison.htm

Cardiovascular Health Library - Education Resources - Heart & Vascular Institute - Willis-Knighton Health System - ShreveportCardiovascular Health Library - Education Resources - Heart & Vascular Institute - Willis-Knighton Health System - Shreveport

The hormone cortisol is always affected but aldosterone may be low as well. Addison disease may be:. *Primary Addison disease- ...
more infohttps://www.wkhs.com/Heart/Education/Library.aspx?chunkiid=12074

Addisons Disease - Articles on Medical Diseases and ConditionsAddison's Disease - Articles on Medical Diseases and Conditions

... it has been suggested that aldosterone should be measured as well as cortisol. Aldosterone levels should increase in pituitary ... Plasma aldosterone is usually decreased and plasma renin is elevated. There often is a normochromic-normocytic mild anemia and ... due to concurrent aldosterone deficiency). One investigator reported hypercalcemia in 6% of patients. There occasionally may be ...
more infohttp://med-life.net/2009/12/22/addisons-disease/

Addison Disease | TriStar Southern HillsAddison Disease | TriStar Southern Hills

The hormone cortisol is always affected but aldosterone may be low as well. Addison disease may be:. *Primary Addison disease- ...
more infohttps://tristarsouthernhills.com/hl/?/12074/Addison-s-disease

DMOZ - Health: Conditions and Diseases: Endocrine Disorders: Adrenal: Addisons DiseaseDMOZ - Health: Conditions and Diseases: Endocrine Disorders: Adrenal: Addison's Disease

... the hormone aldosterone. Addisons disease refers specifically to primary adrenal insufficiency, in which the adrenal glands ... the hormone aldosterone. Addisons disease refers specifically to primary adrenal insufficiency, in which the adrenal glands ...
more infohttp://dmoztools.net/Health/Conditions_and_Diseases/Endocrine_Disorders/Adrenal/Addison%27s_Disease/

Addison disease: blood chemistryAddison disease: blood chemistry

... aldosterone. Primary adrenal insufficiency is usually not apparent until 90% of the adrenal cortex has been destroyed. The most ...
more infohttp://www.openanesthesia.org/addison_disease_blood_chemistry/

Aldosterone - WikipediaAldosterone - Wikipedia

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 ...
more infohttps://en.wikipedia.org/wiki/Aldosterone

Aldosterone escape - WikipediaAldosterone escape - Wikipedia

In physiology, aldosterone escape is a term that has been used to refer to two distinct phenomena involving aldosterone that ... Aldosterone initially results in an increase in Na+ reabsorption in these patients through stimulation of ENaC channels in ... This is the proposed mechanism of "mineralocorticoid escape" for how patients with increased levels of aldosterone are able to ... The inability of ACE inhibitor therapy to reliably suppress aldosterone release, for example, in patients with heart failure or ...
more infohttps://en.wikipedia.org/wiki/Aldosterone_escape

Aldosterone and Renin | SpringerLinkAldosterone and Renin | SpringerLink

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 ...
more infohttps://link.springer.com/chapter/10.1007/978-1-4684-4817-7_5

Aldosterone and ReninAldosterone and Renin

Renin is an enzyme that controls aldosterone production. Aldosterone and renin tests help diagnose primary (Conn syndrome) and ... Aldosterone is a hormone that helps regulate blood pressure. ... Aldosterone may be measured in the blood or in a 24-hour urine ... Aldosterone and renin tests are used to evaluate whether the adrenal glands are producing appropriate amounts of aldosterone ... The aldosterone stimulation test, also called ACTH stimulation, tests aldosterone and cortisol to determine if someone has ...
more infohttps://labtestsonline.org/tests/aldosterone-and-renin

Aldosterone News & OpinionAldosterone News & Opinion

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 ...
more infohttps://www.empowher.com/condition/aldosterone/news

Aldosterone - WikipediaAldosterone - Wikipedia

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 ...
more infohttps://en.m.wikipedia.org/wiki/Aldosterone

Salivary Aldosterone Testing Now Available from SalimetricsSalivary Aldosterone Testing Now Available from Salimetrics

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 ...
more infohttp://www.prweb.com/releases/prwebsalivary_aldosterone/salimetrics/prweb9970342.htm

Aldosterone | Definition of Aldosterone at Dictionary.comAldosterone | Definition of Aldosterone at Dictionary.com

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 ...
more infohttps://www.dictionary.com/browse/aldosterone

Aldosterone - DrugBankAldosterone - DrugBank

Aldosterone may increase the hypokalemic activities of Indapamide.. Approved. Indinavir. The serum concentration of Aldosterone ... Aldosterone may increase the fluid retaining activities of Stanolone.. Illicit, Investigational. Stanozolol. Aldosterone may ... At the late distal tubule and collecting duct, aldosterone has two main actions: 1) aldosterone acts on mineralocorticoid ... Aldosterone may increase the hypokalemic activities of Etacrynic acid.. Approved. Etanercept. The risk or severity of adverse ...
more infohttps://www.drugbank.ca/drugs/DB04630

Heart-and-Stroke-Encyclopedia - aldosteroneHeart-and-Stroke-Encyclopedia - aldosterone

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 ...
more infohttp://www.heart.org/HEARTORG/Encyclopedia/Heart-and-Stroke-Encyclopedia_UCM_445084_Encyclopedia.jsp?levelSelected=1&title=aldosterone

Selective Aldosterone Receptor AntagonistSelective Aldosterone Receptor Antagonist

... , 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 ...
more infohttps://fpnotebook.com/cv/Pharm/SlctvAldstrnRcptrAntgnst.htm

Cortisol/Aldosterone levels help - Adrenal Insufficiency - MedHelpCortisol/Aldosterone levels help - Adrenal Insufficiency - MedHelp

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 ...
more infohttps://www.medhelp.org/posts/Adrenal-Insufficiency/Cortisol-Aldosterone-levels-help/show/3000941

Aldosterone - wikidocAldosterone - wikidoc

The secretion of aldosterone has a diurnal rhythm.[4] Control of aldosterone release from the Adrenal Cortex. *The role of the ... The last part is either mediated by the aldosterone synthase (for aldosterone) or by the 11β-hydroxylase (for corticosterone). ... Diurnal variation of aldosterone and plasma renin activity: timing relation to melatonin and cortisol and consistency after ... Aldosterone synthesis is stimulated by several factors: *by increased plasma angiotensin II, ACTH, or potassium levels, which ...
more infohttps://www.wikidoc.org/index.php/Aldosterone

Aldosterone and ReninAldosterone and Renin

... and what the results of aldosterone and renin tests might mean ... Describes when aldosterone and renin tests are requested, how ... Aldosterone levels are sometimes used in people suspected of having poor adrenal function. Some doctors use aldosterone and ... To see if your aldosterone or renin levels are abnormal; to detect hyperaldosteronism (overproduction of aldosterone) or ... Angiotensin II then regulates the release of aldosterone. Normally when renin increases, aldosterone increases; when renin is ...
more infohttps://labtestsonline.org.uk/tests/aldosterone-and-renin

New aspects of rapid aldosterone signaling.  - PubMed - NCBINew aspects of rapid aldosterone signaling. - PubMed - NCBI

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 ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/19549592?dopt=Abstract

yo-yo aldosterone levels - Thyroid Disorders - MedHelpyo-yo aldosterone levels - Thyroid Disorders - MedHelp

... 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 ...
more infohttp://www.medhelp.org/posts/Thyroid-Disorders/yo-yo-aldosterone-levels/show/793905

Human Endothelium: Target for Aldosterone | HypertensionHuman Endothelium: Target for Aldosterone | Hypertension

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 ...
more infohttp://hyper.ahajournals.org/content/43/5/952.short

Does Sodium Consumption Affect Aldosterone? | LIVESTRONG.COMDoes Sodium Consumption Affect Aldosterone? | LIVESTRONG.COM

Aldosterone. Aldosterone, a hormone secreted by the outer layer of your adrenal glands, stimulates your kidneys to absorb more ... "sodium intake aldosterone,sodium concentration aldosterone]"} Get the latest tips on diet, exercise and healthy living.. ... Aldosterone, a hormone released by your adrenal glands in response to blood sodium concentrations, can be affected by sodium ... Aldosterone secretion is increased by several mechanisms, including decreased blood flow to your kidneys, high serum potassium ...
more infohttps://www.livestrong.com/article/523374-does-sodium-consumption-affect-aldosterone/
  • Salimetrics' list of measurable biomarkers in saliva has expanded once again with the addition of an assay for salivary aldosterone. (prweb.com)
  • 1) Screening for PA among hypertensive patients is important due ​to its association with risk for cardiovascular disease and renal damage, (1) and non-invasive salivary aldosterone measurements have recently been explored as a means to facilitate this screening. (salimetrics.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)
  • The increased potassium level works to regulate aldosterone synthesis by depolarizing the cells in the zona glomerulosa, which opens the voltage-dependent calcium channels. (wikipedia.org)
  • Steroidogenesis , showing aldosterone synthesis at upper-right corner. (wikipedia.org)
  • Raised plasma aldosterone and natriuretic peptides in atrial fibrillation. (nih.gov)
  • At follow-up, 93 patients had SR. Heart rhythm at follow-up visit (SR/AF), plasma aldosterone, plasma N-terminal pro Brain Natriuretic Peptide (Nt-proBNP), plasma N-terminal pro Atrial Natriuretic Peptide (Nt-proANP), LVEF, medication, and clinical characteristics were recorded. (nih.gov)
  • 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)
  • In women who have recently had a heart attack and have a systolic heart failure(blood pumping problems) that is causing symptoms, adding the aldosterone antagonist eplerenone to standard treatment reduces hospitalization and improves survival. (simstat.com)
  • Aldosterone enters a target cell and binds MR, which translocates into the nucleus and regulates gene transcription. (genome.jp)
  • 2009). Saliva as a medium for aldosterone measurement in repeated sampling studies. (prweb.com)
  • 4) Circulating aldosterone, not bound to serum proteins, enters saliva by passive diffusion. (salimetrics.com)
  • Aldosterone was first isolated by Simpson and Tait in 1953. (wikipedia.org)
  • The last parts are mediated either by the aldosterone synthase (for aldosterone) or by the 11β-hydroxylase (for corticosterone). (wikipedia.org)
  • The last part is either mediated by the aldosterone synthase (for aldosterone ) or by the 11β-hydroxylase (for corticosterone ). (wikidoc.org)
  • 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)
  • No specific binding protein for aldosterone has been identified in blood. (salimetrics.com)
  • The risk or severity of adverse effects can be increased when Aldosterone is combined with 1,10-Phenanthroline. (drugbank.ca)
  • The risk or severity of adverse effects can be increased when Aceclofenac is combined with Aldosterone. (drugbank.ca)