11 beta,18,21-Trihydroxypregn-4-ene-3,20-dione.
An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.
A mitochondrial cytochrome P450 enzyme that catalyzes the 11-beta-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11B1 gene, is important in the synthesis of CORTICOSTERONE and HYDROCORTISONE. Defects in CYP11B1 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).
An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1437)
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
A mitochondrial cytochrome P450 enzyme that catalyzes the 18-hydroxylation of steroids in the presence of molecular oxygen and NADPH-specific flavoprotein. This enzyme, encoded by CYP11B2 gene, is important in the conversion of CORTICOSTERONE to 18-hydroxycorticosterone and the subsequent conversion to ALDOSTERONE.
A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.
A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.
The narrow subcapsular outer zone of the adrenal cortex. This zone produces a series of enzymes that convert PREGNENOLONE to ALDOSTERONE. The final steps involve three successive oxidations by CYTOCHROME P-450 CYP11B2.
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.
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.
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.
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.

Aldosterone synthase deficiency type I with no documented homozygous mutations in the CYP11B2 gene. (1/16)

This case report concerns a girl born from non-consanguineous parents and hospitalized in another hospital at the age of 14 days because of a severe salt-losing syndrome (Na=125, K=8.6 mEq/l). In spite of normal genitalia, diagnosis of 21-hydroxylase deficiency was assessed on the basis of a slightly increased 17-OH-progesterone serum level (6.4 ng/ml). The onset of both hydrocortisone and 9alpha-fluorohydrocortisone therapy was followed by a resolution of the clinical picture. At the age of 60 days she was admitted to our clinic for a re-evaluation of the diagnosis. Steroid hormone serum levels were measured after withdrawal of therapy and diagnosis of corticosterone methyl oxidase (CMO) deficiency type I was definitely established in the light of the biochemical results: i.e. very low 18-hydroxycorticosterone (18-OH-B) serum levels (20 pg/ml), an abnormally high corticosterone/18-OH-B serum ratio (306.5) and an abnormally low 18-OH-B/aldosterone serum ratio (2.1). This autosomal recessively inherited disorder can be differentiated from CMO type II and other salt-wasting syndromes only on the basis of the serum steroid hormone pattern. After establishing the diagnosis of CMO I deficiency, hydrocortisone therapy was withdrawn whilst treatment with 9alpha-fluorohydrocortisone was begun again, with a satisfactory clinical and metabolic impact. Direct sequences of the patient's DNA were able to identify only a (heterozygous) amino acid substitution in exon 7 of that gene, which is known to have only a small effect on enzyme activity and cannot be the only cause of the patient's phenotype: valine-386-alanine (V386A) GTG-->GcG. No homozygous mutations in the CYP11B2 gene were observed. This is the first report of a patient with CMO type I who does not carry any homozygous mutation in the entire CYP11B2 alleles, whereas some cases with no mutations in this gene have already been reported in CMO II. The present study seems to be inconsistent with the previously reported correlation of the phenotype and genotype in CMO type I. A reasonable question that might be raised on the basis of our findings in this case report is whether other genes, apart from CYP11B2, are involved in the regulation of terminal aldosterone synthesis.  (+info)

Mutations in aldosterone synthase gene of Milan hypertensive rats: phenotypic consequences. (2/16)

Using in vitro and in vivo methods, we have demonstrated increased sensitivity of adrenocortical steroidogenesis to ACTH in Milan hypertensive (MHS) compared with normotensive (MNS) rats and have investigated whether this is caused by mutations of steroidogenic enzymes. Genes encoding aldosterone synthase (CYP11B2) and 11beta-hydroxylase (CYP11B1) in MHS and MNS have been cloned and sequenced. Nucleotide 752 (G) in exon 4 of MHS CYP11B2 differs from that of MNS (A); CYP11B1 sequences were identical. The nucleotide 752 mutation caused a Q251R substitution in the amino acid sequence of MHS CYP11B2. The phenotype of MHS CYP11B2 alleles, when expressed in COS-1 cells, differed from that of MNS alleles. The relative activities of the three reactions catalyzed by CYP11B2 (11beta-hydroxylation of deoxycorticosterone, 18-hydroxylation of corticosterone, and dehydrogenation of 18-hydroxycorticosterone) were estimated after incubation of transfected cells with [(14)C]deoxycorticosterone and analysis of radioactivity associated with deoxycorticosterone, corticosterone, 18 hydroxycorticosterone, and aldosterone. Both 11- and 18-hydroxylase activities were lower (19 and 12%, respectively; P < 0.01 and P < 0.05) in cells transfected with MHS compared with MNS alleles, whereas 18-oxidase activity was 42% higher (P < 0.01). To assess the significance of the CYP11B2 mutation in vivo, DNA from F2 hybrid MHS x MNS rats was genotyped. MHS alleles were associated with lower urine volumes in both sexes, lower ventricle weights in male rats, but no difference in systolic or diastolic blood pressures between the sexes. We conclude that a mutation in CYP11B2 may affect aldosterone secretion in MHS; however, under normal environmental circumstances, we were unable to demonstrate any influence of this mutation on blood pressure.  (+info)

Stereological and functional investigations on isolated adrenocortical cells. III. Zona glomerulosa cells of chronically ACTH-treated rats. (3/16)

Prolonged (5 day) treatment of rats with high doses of ACTH caused a significant reduction in the plasma concentration of aldosterone and a notable rise in that of corticosterone. Outer subcapsular (zona glomerulosa [ZG]) adrenocortical cells were isolated, and their morphology and secretory activity was investigated. ACTH pretreatment induced a marked hypertrophy of ZG cells which was coupled with significant increases in the volume of the mitochondrial compartment and in the surface area per cell of mitochondrial cristae and AER tubules, as well as with a striking lipid droplet depletion. Mitochondrial cristae were found to change from a tubulo-laminar to a tubulo-convolute configuration. Despite their hypertrophy, ZG cells from ACTH-pretreated rats displayed a conspicuous decrease in both basal and stimulated overall production of post-pregnenolone steroids, which was ascribed to the depletion of their stores of steroid hormone precursors (i.e. cholesterol and cholesterol esters contained in the lipid droplets). However, both basal and stimulated secretion of aldosterone was doubled, suggesting that chronic ACTH treatment induces in ZG cells an increased availability of monoxygenase II, the enzyme involved in the transformation of 18-hydroxycorticosterone into aldosterone. In the light of these findings, the drop in the plasma level of aldosterone observed in rats after prolonged treatment with ACTH is assumed to be due to an enhanced metabolism of aldosterone, possibly at the hepatic level.  (+info)

Altered responses of plasma 18-hydroxycorticosterone and aldosterone to angiotensin II and adrenocorticotropin in patients with a 18-hydroxycorticosterone-producing tumor. (4/16)

Plasma 18-hydroxycorticosterone (18-OHB) and aldosterone responses to angiotensin II (AII) and ACTH were examined in 2 patients with a 18-OHB-producing tumor (18-OHBPT) versus those in 8 patients with a aldosterone-producing adenoma (APA), 7 patients with low renin essential hypertension (LREH) and 10 normal subjects. Plasma 18-OHB and aldosterone levels and the 18-OHB: aldosterone ratio were high in patients with an APA and normal in patients with LREH. In patients with a 18-OHBPT, plasma 18-OHB and aldosterone levels were high and normal, respectively, resulting in a 2-fold greater 18-OHB: aldosterone ratio than that in patients with an APA. Patients with an APA had a blunted response of plasma 18-OHB and aldosterone to AII and a supranormal response of these corticoids to ACTH. Patients with LREH had a supranormal response of plasma 18-OHB and aldosterone to AII and a normal response of these corticoids to ACTH. In patients with a 18-OHBPT the responses of both plasma 18-OHB and aldosterone to AII and ACTH closely resembled those in patients with an APA but not in patients with LREH. These data suggest that 18-OHBPT may be a variant of aldosteronomas, producing a large amount of 18-OHB and a small amount of aldosterone.  (+info)

Effects of corticotropin-releasing factor (CRF) on aldosterone and 18-hydroxycorticosterone in essential hypertension and primary aldosteronism. (5/16)

The effects of ovine corticotropin releasing factor (o-CRF) on plasma aldosterone, 18-OH-corticosterone (18-OHB), plasma adrenocorticotropin (ACTH) and cortisol were determined in eight patients with primary aldosteronism, six with aldosterone-producing adenoma (APA) and two with idiopathic hyperaldosteronism (IHA). The results were compared with those in six normal subjects and eleven patients with essential hypertension (EHT, 5 with low renin and 6 with normal renin). In patients with APA, the peak plasma aldosterone and 18-OHB responses to 100 micrograms iv of o-CRF (226% and 113% increase from baseline, respectively) were greater than those in EHT and normal subjects. The net integrated aldosterone and 18-OHB responses (840 +/- 156, and 419 +/- 121 ng/dl.hr, respectively) were also significantly greater (p less than 0.01) in APA than those in normals and EHT. In two patients with IHA, both the peak and net integrated aldosterone response were smaller than those in APA, in spite of nearly identical plasma ACTH and cortisol responses. These results suggest that augmented responses of mineralocorticoids to o-CRF may be characteristic of aldosteronism due to APA, mediated by CRF-induced ACTH, and possibly other proopiomelanocortin (POMC)-derived peptides.  (+info)

The renal, cardiovascular and hormonal actions of human atrial natriuretic peptide in man; effects of indomethacin. (6/16)

The renal, cardiovascular and hormonal effects of intravenous infusion of alpha-human atrial natriuretic polypeptides (alpha-hANP) at the concentrations of 0.0125, 0.025, 0.05, 0.1 microgram kg-1 min-1 for 20 min was studied in six male volunteers before and after indomethacin administration (150 mg day-1, three times daily for 3 days). Dose-dependent diuresis and natriuresis were observed in all subjects between the concentrations of 0.025 and 0.1 microgram kg-1 min-1, which were not influenced by indomethacin. Diastolic blood pressure decreased significantly (P less than 0.05) at the higher dose (0.05 microgram kg-1 min-1) of alpha-hANP, which was attenuated by indomethacin pretreatment. The plasma concentration of the immunoreactive alpha-hANP was 73.7 +/- 25 pg ml-1 on the control in subjects taking 200 mEq day-1 of sodium, and significant diuresis occurred when plasma concentration reached approximately 330.5 +/- 74.4 pg ml-1. alpha-hANP infusion caused a dose-dependent increase in cyclic GMP, no significant changes in plasma aldosterone and 18-hydroxycorticosterone, which were not influenced by indomethacin pretreatment. Plasma renin did not change in response to alpha-hANP infusion, which was significantly decreased (P less than 0.05) after indomethacin pretreatment. These results support that the renal effects of alpha-hANP may be exerted by prostaglandin-independent mechanisms. The renal effects occur at lower doses, and cardiovascular changes occur at higher doses of alpha-hANP.  (+info)

An adrenocortical tumor secreting weak mineralocorticoids. (7/16)

An adrenocortical carcinoma (15.5 g) secreting excessive amounts of steroids with weak mineralocorticoid activity in a 25-year-old woman was studied with particular reference to its in vivo and in vitro secretions of steroids. Severe hypertension, occasional low serum potassium and suppressed PRA were the major clinical findings, and were improved with removal of the tumor. In the preoperative stage, plasma levels of 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, corticosterone and 18-hydroxycorticosterone were all increased. However, the plasma level of aldosterone was repeatedly normal. Although plasma levels of pregnenolone, 17-hydroxypregnenolone, progesterone and 17-hydroxyprogesterone were very high, those of other late step steroids, i.e. 11-deoxycortisol, cortisol, dehydroepiandrosterone, androstenedione and testosterone were almost normal. From these findings, a major etiological role of weak mineralocorticoids such as 11-deoxycorticosterone, 18-hydroxycorticosterone and corticosterone in her hypertension was suggested. Pregnenolone and 17-hydroxypregnenolone in tumor tissue were increased, but 11-deoxycorticosterone, corticosterone, aldosterone, cortisol and adrenal androgens such as dehydroepiandrosterone, androstenedione and testosterone were below normal or low normal. In vitro production of 11-deoxycorticosterone, aldosterone or cortisol by the tumor tissue slices was very low and scarcely responded to synthetic ACTH.  (+info)

Adrenal steroid responses to ACTH in glucocorticoid-suppressible aldosteronism. (8/16)

To investigate adrenal responses to adrenocorticotrophin (ACTH), we infused graded doses of ACTH (1.25 to 20.0 mIU/30 minutes) in normal subjects, patients with low-renin essential hypertension (LREH), primary aldosteronism (PA), and glucocorticoid-suppressible hyperaldosteronism (GSH). Plasma aldosterone, cortisol, corticosterone, and 18-hydroxycorticosterone were measured. The results revealed a greater increase in the plasma aldosterone and 18-hydroxycorticosterone levels evoked by ACTH in the GSH group than in any other group, which suggested enhanced responsiveness of the aldosterone-producing cells to ACTH and a probable adrenal abnormality.  (+info)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Zona glomerulosa is a region of the adrenal gland, specifically the outer portion of the adrenal cortex. It is responsible for producing mineralocorticoids, with the principal one being aldosterone. Aldosterone helps regulate electrolyte and fluid balance in the body by increasing the reabsorption of sodium ions and water in the distal nephron of the kidney while promoting the excretion of potassium ions. This process assists in maintaining blood pressure and volume within normal ranges. The zona glomerulosa's function is primarily under the control of the renin-angiotensin-aldosterone system (RAAS).

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

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

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

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

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

Medical Definition:

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

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

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

... serves as an intermediate in the synthesis of aldosterone by the enzyme aldosterone synthase in the ... 18-Hydroxycortisol Aldosterone synthase Reddish MJ, Guengerich FP (August 2019). "Human cytochrome P450 11B2 produces ... 18-Hydroxycorticosterone is an endogenous steroid. It is a derivative of corticosterone. ... Izumi Y (July 2010). "[18-Hydroxycorticosterone (18-OH-B)]". Nihon Rinsho. Japanese Journal of Clinical Medicine (in Japanese ...
18-Hydroxycortisol 18-Hydroxycorticosterone "Familial hyperaldosteronism". Genetics home reference. April 2014. Retrieved 8 ...
Consequently, levels of DOC, corticosterone, and 18-hydroxycorticosterone are elevated. Although these precursors of ...
18 (1): 117-24. doi:10.1046/j.1460-9568.2003.02734.x. PMID 12859344. S2CID 42753764. Labrie C, Simard J, Zhao HF, Belanger A, ... 2007). "Measurement of 18-Hydroxycorticosterone During Adrenal Vein Sampling for Primary Aldosteronism". Journal of Clinical ...
... is an endogenous steroid. 18-hydroxycortisol has been proposed as a biomarker for certain diseases. In ... Cortisol 18-Hydroxycorticosterone Aldosterone synthase Steroid 11β-hydroxylase 6β-Hydroxycortisol Lenders J, Williams T, ... In healthy subjects, the biosynthesis of 18-hydroxycortisol is low. The highest synthesis of 18-hydroxycortisol was found in ... Chiba H (July 2010). "18-Hydroxycortisol, 18-oxocortisol, and 6beta-hydroxycortisol". Nihon Rinsho. Japanese Journal of ...
18 (1): 41-78. doi:10.1089/vim.2005.18.41. PMC 1224723. PMID 15802953. Robson PJ, Blannin AK, Walsh NP, Castell LM, Gleeson M ( ... I 18-hydroxylation and 18hydroxy dehydrogenation. II beta-hydroxylation". Acta Endocrinol. 69 (4): I 701-717, II 718-730. doi: ... 18 (4): 301-9. PMID 3084123. Mikosha AS, Pushkarov IS, Chelnakova IS, Remennikov GY (1991). "Potassium Aided Regulation of ... "The effect of sodium deprivation and of angiotensin II infusion on the peripheral plasma concentrations of 18- ...
In humans, 18-OH-DOC is a weak mineralocorticoid. It may be increased in 17α-hydroxylase (CYP17A1) deficiency, in aldosterone ... Excessive secretion of 18-OH-DOC can cause mineralocorticoid excess syndrome, although these cases are very rare. Fujii S, ... 18-hydroxydeoxycorticosterone at the U.S. National Library of Medicine Medical Subject Headings (MeSH) v t e (Articles without ... 18-Hydroxy-11-deoxycorticosterone (also known as 18-OH-DOC, 18,21-dihydroxyprogesterone, and 18,21-dihydroxypregn-4-ene-3,20- ...
18-hydroxypregn-4-ene-3,20-dione [5] 21-Deoxycortisol = 11β,17α-dihydroxypregn-4-ene-3,20-dione, 21-Deoxycortisone = 17α- ... 18,20-trione Corticosterone (17-deoxycortisol) = 11β,21-dihydroxypregn-4-ene-3,20-dione Cortisol (hydrocortisone) = 11β,17α,21- ... 18,21-dihydroxypregn-4-ene-3,20-dione [4] 18-Hydroxycorticosterone = 11β,18,21-trihydroxypregn-4-ene-3,20-dione 18- ...
In enzymology, a corticosterone 18-monooxygenase (EC 1.14.15.5) is an enzyme that catalyzes the chemical reaction ... "ENZYME - 1.14.15.5 corticosterone 18-monooxygenase". enzyme.expasy.org. Archived from the original on 2022-08-20. Retrieved ... "PhytoMine: GOTerm GO:0047783 corticosterone 18-monooxygenase activity GO". phytozome-next.jgi.doe.gov. Archived from the ... The systematic name of this enzyme class is corticosterone,reduced-adrenal-ferredoxin:oxygen oxidoreductase (18-hydroxylating ...
18-hydroxydesoxycorticosterone MeSH D06.472.040.585.745 - pregnenolone MeSH D06.472.040.585.745.500 - 17-alpha- ... 18-hydroxycorticosterone MeSH D06.472.040.585.353.825 - tetrahydrocortisol MeSH D06.472.040.585.478 - 17-hydroxycorticosteroids ...
... a corticosteroid 5α-Dihydroaldosterone Dihydrocortisone Hydrocortisone Humulone 18-Hydroxycorticosterone Isohumulone This set ...
18-hydroxycorticosterone MeSH D04.808.745.745.654.252 - cortodoxone MeSH D04.808.745.745.654.339 - desoxycorticosterone MeSH ... D04.808.745.745.654.339.400 - 18-hydroxydesoxycorticosterone MeSH D04.808.745.745.654.473 - flurandrenolone MeSH D04.808. ...
The weak 18-hydroxylase activity of CYP11B1 explains why an adrenal with suppressed CYP11B2 expression continues to synthesize ... Nicod J, Dick B, Frey FJ, Ferrari P (February 2004). "Mutation analysis of CYP11B1 and CYP11B2 in patients with increased 18- ... Fisher A, Friel EC, Bernhardt R, Gomez-Sanchez C, Connell JM, Fraser R, Davies E (September 2001). "Effects of 18-hydroxylated ... The CYP11B1 isozyme has strong 11β-hydroxylase activity, but the activity of 18-hydroxylase is only one-tenth of CYP11B2. ...
The 18-hydroxylase activity consists in catalyzing sequential hydroxylations of the steroid angular methyl group at C18. ... May 1997). "CMO I deficiency caused by a point mutation in exon 8 of the human CYP11B2 gene encoding steroid 18-hydroxylase ( ... Aldosterone synthase is the enzyme that has steroid 18-hydroxylase activity as well as steroid 11 beta-hydroxylase activity. ... The corticosterone methyl oxidase deficiencies both share this effect however type I causes an overall deficiency of 18- ...
18-Hydroxycorticosterone serves as an intermediate in the synthesis of aldosterone by the enzyme aldosterone synthase in the ... 18-Hydroxycortisol Aldosterone synthase Reddish MJ, Guengerich FP (August 2019). "Human cytochrome P450 11B2 produces ... 18-Hydroxycorticosterone is an endogenous steroid. It is a derivative of corticosterone. ... Izumi Y (July 2010). "[18-Hydroxycorticosterone (18-OH-B)]". Nihon Rinsho. Japanese Journal of Clinical Medicine (in Japanese ...
aldosterone, angiotensin II, dopamine, essential low-renin hypertension, 18-hydroxycorticosterone, metoclopramide, primary ... 3. Dopamine reduced the maximal increase of aldosterone and of 18-OH-B after angiotensin II to 259 ± 48 (sem) pg/ml and 511 ± ... Plasma levels of 18-OH-DOC, corticosterone and cortisol were not affected by the stimuli applied. ... 2. As compared with the other groups, an exaggerated angiotensin II-induced response of plasma aldosterone and 18-OH-B levels ...
18-Hydroxycorticosterone, 18-hydroxycortisol and 18-oxocortisol in the diagnosis of primary aldosteronism and its subtypes.. P ... 18-Hydroxycorticosterone, 18-hydroxycortisol and 18-oxocortisol in the diagnosis of primary aldosteronism and its subtypes. (. ... 18-Hydroxycorticosterone, 18-hydroxycortisol and 18-oxocortisol in the diagnosis of primary aldosteronism and its subtypes. ... We evaluated the role of serum 18-hydroxycorticosterone (s18OHB) and urinary and serum 18-hydroxycortisol (u and s18OHF) and 18 ...
18-Hydroxycorticosterone. On-line free medical diagnosis assistant. Ranked list of possible diseases from either several ...
Bilateral hyperplasia of the zona fasciculata occurs, and high levels of novel 18-hydroxysteroids appear in the urine. Adenoma ... The enzyme aldosterone synthase is encoded by the gene CYP11B2 and has 11β-hydroxylase, 18-hydroxylase, and 18- ... The result is ACTH-dependent aldosterone production and production of 17-hydroxylated analogues of 18-hydroxycortisol under ... Numerous aldosterone precursors, including deoxycorticosterone and 18-hydroxycorticosterone, have mineralocorticoid activity ...
Aldosterone deficiency due to deficiency of steroid 18-hydroxylase. *Aldosterone deficiency due to deficiency of steroid 18- ... and the conversion of 18-hydroxycorticosterone to aldosterone.. The CYP11B2 gene mutations that cause corticosterone ...
Effect of domperidone, an extracerebral inhibitor of dopamine receptors, on thyrotropin, prolactin, renin, aldosterone, and 18- ... hydroxycorticosterone secretion in man. J. Clin. Endocrinol. Metab., 54: 869-871.. CrossRef ...
Brief report: Measurement of 18-hydroxycorticosterone during adrenal vein sampling for primary aldosteronism. Auchus, R. J., ... 18, 5, p. 458-467 10 p.. Research output: Contribution to journal › Article › peer-review ...
3,5,6-TRICHLORO-2-PYRIDINOL (TCPY ...
18-Hydroxycorticosterone. O. 2. H. 2. O. Accumulation. Corticosterone. O. 2. H. 2. O. 11b,21-Dihydroxy-5b-. pregnane-3,20-dione ... 5b-pregnan-18-al. NADPH. 3a,11b,21-Trihydroxy-20-oxo-. 5b-pregnan-18-al. NADP. NADP. Aldosterone. NADPH. Accumulation. ...
Question 18 of 30 18. Question A 64-year old woman with a history of thyroidectomy for Graves disease has been taking thyroxine ...
18-hydroxycorticosterone, and cortisol. Metabolic pathways associated with variable rates of disease progression included ...
The highest excretion occurs at midday, approximately 18 hours after peak potassium ingestion at the evening meal. ... They will have an increased serum ratio of 18-hydroxycorticosterone to aldosterone. ...
Blood was also drawn for measurement of serum aldosterone and 18-hydroxycorticosterone levels. Results of the above work-up ... 18-hydroxycorticosterone 24 ng/dL (reference: 5 to 80), urine aldosterone 4.6 kg/24 h (reference: 2.3 to 21), and urine ... The patients voiced no complaints in the 18 months thereafter; periodic ABPMs were performed during the follow-up, and minor ...
In addition to this activity, the 18 or 19-hydroxylation of steroids and the aromatization of androstendione to estrone have ... Preferentially catalyzes the conversion of 11-deoxycorticosterone to aldosterone via corticosterone and 18- ... hydroxycorticosterone.. Gene Name. CYP11B2. Uniprot ID. P19099. Uniprot Name. Cytochrome P450 11B2, mitochondrial. Molecular ...
... hydroxycorticosterone in patients with primary aldosteronism. J Clin Endocrinol Metab 49: 87‐91, 1979. ... J Hum Hypertension 18: 47‐51, 2004.. 83.. Fallo F , Veglio F , Bertello C , Sonino N , Della Mea P , Ermani M , Rabbia F , ... J Endocrinol Invest 18: 370‐373, 1995.. 368.. Takeda Y , Miyamori I , Iki K , Inaba S , Furukawa K , Hatakeyama H , Yoneda T , ... 18.. Banks WA , Kastin AJ , Biglieri EG , Ruiz AE . Primary adrenal hyperplasia: A new subset of primary aldosteronism. J Clin ...
... corticosterone and 18-hydroxycorticosterone); CYP11B2 gene transcription is under control of angiotensin II. ...
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B1.650.940.800.575.100.18 Agave B1.650.940.800.575.100.18.249 B1.650.940.800.575.100.99.60.32 Agglutination G2.111.87.26 G2.111 ... 18-Hydroxydesoxycorticosterone D4.808.745.745.654.339.400 D4.210.500.745.745.654.339.400 19-Iodocholesterol D4.808.247.222. ... 18-Hydroxycorticosterone D4.808.745.745.654.237.400 D4.210.500.745.745.654.237.400 ...
B1.650.940.800.575.100.18 Agave B1.650.940.800.575.100.18.249 B1.650.940.800.575.100.99.60.32 Agglutination G2.111.87.26 G2.111 ... 18-Hydroxydesoxycorticosterone D4.808.745.745.654.339.400 D4.210.500.745.745.654.339.400 19-Iodocholesterol D4.808.247.222. ... 18-Hydroxycorticosterone D4.808.745.745.654.237.400 D4.210.500.745.745.654.237.400 ...
B1.650.940.800.575.100.18 Agave B1.650.940.800.575.100.18.249 B1.650.940.800.575.100.99.60.32 Agglutination G2.111.87.26 G2.111 ... 18-Hydroxydesoxycorticosterone D4.808.745.745.654.339.400 D4.210.500.745.745.654.339.400 19-Iodocholesterol D4.808.247.222. ... 18-Hydroxycorticosterone D4.808.745.745.654.237.400 D4.210.500.745.745.654.237.400 ...
B1.650.940.800.575.100.18 Agave B1.650.940.800.575.100.18.249 B1.650.940.800.575.100.99.60.32 Agglutination G2.111.87.26 G2.111 ... 18-Hydroxydesoxycorticosterone D4.808.745.745.654.339.400 D4.210.500.745.745.654.339.400 19-Iodocholesterol D4.808.247.222. ... 18-Hydroxycorticosterone D4.808.745.745.654.237.400 D4.210.500.745.745.654.237.400 ...
B1.650.940.800.575.100.18 Agave B1.650.940.800.575.100.18.249 B1.650.940.800.575.100.99.60.32 Agglutination G2.111.87.26 G2.111 ... 18-Hydroxydesoxycorticosterone D4.808.745.745.654.339.400 D4.210.500.745.745.654.339.400 19-Iodocholesterol D4.808.247.222. ... 18-Hydroxycorticosterone D4.808.745.745.654.237.400 D4.210.500.745.745.654.237.400 ...
... the conversion of corticosterone to 18-hydroxycorticosterone, and the conversion of 18-hydroxycorticosterone to aldosterone. ...
Corticosterone 18-monooxygenase deficiency. CMO type I deficiency is an autosomal recessive disorder caused by a defect in the ... In CMO II deficiency, aldosterone can be low or normal, but at the expense of increased secretion of 18-OHB. These patients ... In CMO II deficiency, aldosterone can be low or normal, but at the expense of increased secretion of 18-OHB. These patients ... These patients have an increased ratio of corticosterone to 18-OHB (Portrat-Doyen et al., 1998). The CYP11B2 gene product also ...
  • 1. Plasma aldosterone, 18-hydroxycorticosterone (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC), corticosterone, cortisol and prolactin levels were determined during an angiotensin II infusion at increasing rates both with and without a simultaneous infusion of dopamine in seven normotensive subjects, in ten patients with essential hypertension, and in ten patients with primary aldosteronism. (portlandpress.com)
  • Plasma levels of 18-OH-DOC, corticosterone and cortisol were not affected by the stimuli applied. (portlandpress.com)
  • The aldosterone synthase enzyme is involved in a series of three chemical reactions that produce aldosterone from other (precursor) molecules: the conversion of 11-deoxycorticosterone to corticosterone, the conversion of corticosterone to 18-hydroxycorticosterone, and the conversion of 18-hydroxycorticosterone to aldosterone. (medlineplus.gov)
  • 18-Hydroxycorticosterone serves as an intermediate in the synthesis of aldosterone by the enzyme aldosterone synthase in the zona glomerulosa. (wikipedia.org)
  • 18-Hydroxycortisol Aldosterone synthase Reddish MJ, Guengerich FP (August 2019). (wikipedia.org)
  • 2. As compared with the other groups, an exaggerated angiotensin II-induced response of plasma aldosterone and 18-OH-B levels was observed in the five patients with low-renin essential hypertension (LREH) and in five patients with idiopathic hyperaldosteronism (IHA). (portlandpress.com)
  • 5. The exaggerated response to metoclopramide as well as to angiotensin II and its reversion only by pharmacological doses of dopamine are consistent with an increased but ineffective dopamine inhibition of aldosterone and 18-OH-B in LREH and IHA. (portlandpress.com)
  • We evaluated the role of serum 18-hydroxycorticosterone (s18OHB) and urinary and serum 18-hydroxycortisol (u and s18OHF) and 18-oxocortisol (u and s18oxoF) in the diagnosis of PA and its subtypes, aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH). (endocrine-abstracts.org)
  • Numerous aldosterone precursors, including deoxycorticosterone and 18-hydroxycorticosterone, have mineralocorticoid activity and may produce or exacerbate features typical of mineralocorticoid hypertension when present in excessive amounts in various pathologic states. (medscape.com)
  • 18-Hydroxycorticosterone is an endogenous steroid. (wikipedia.org)
  • 18-Hydroxycorticosterone serves as an intermediate in the synthesis of aldosterone by the enzyme aldosterone synthase in the zona glomerulosa. (wikipedia.org)
  • 18-Hydroxycortisol Aldosterone synthase Reddish MJ, Guengerich FP (August 2019). (wikipedia.org)
  • Esta enzima, codificada por el gen CYP11B2, es importante en la conversión de la CORTICOSTERONA en 18-hidroxicorticosterona y la subsiguiente conversión en ALDOSTERONA. (bvsalud.org)
  • A mitochondrial cytochrome P450 enzyme that catalyzes the 18-hydroxylation of steroids in the presence of molecular oxygen and NADPH-specific flavoprotein. (bvsalud.org)