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Chemical Compound Review

AC1NSV9C     (11S)-11-hydroxy-17-(2- hydroxyethanoyl)-10...

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Disease relevance of ALDOSTERONE


Psychiatry related information on ALDOSTERONE


High impact information on ALDOSTERONE


Chemical compound and disease context of ALDOSTERONE


Biological context of ALDOSTERONE


Anatomical context of ALDOSTERONE

  • The ratio of plasma renin activity to urinary aldosterone was used as a measure of the response of the adrenal zona glomerulosa [15].
  • The trophic actions include stimulation of angiotensin II receptors and enzymes of the aldosterone biosynthetic pathway, with corresponding enhancement of the aldosterone secretory capacity of the adrenal gland [25].
  • Performed with a serum potassium measurement, this now reliable test is useful for primary screening and then, in conjunction with renal vein renin studies or an aldosterone profile, for diagnosis or exclusion of surgically curable renovascular or adrenocortical hypertensions [26].
  • Mineralocorticoids, the most prominent of which is aldosterone, also influence the activity of nonepithelial target cells, including vascular smooth muscle cells, by altering intracellular ion transport and content [27].
  • Like their endocrine and neural counterparts, these behaviors are under the control of both excitatory and inhibitory influences arising from changes in osmolality, endocrine factors such as angiotensin and aldosterone, and neural signals from low and high pressure baroreceptors [19].

Associations of ALDOSTERONE with other chemical compounds

  • Atrial peptides also inhibit renal renin secretion and adrenal cortical secretion of aldosterone, and they oppose the vasoconstrictive action of angiotensin II [28].
  • Potassium depletion suppressed plasma aldosterone levels but had no effect on plasma renin activity or on arginine vasopressin or catecholamine levels [29].
  • Recent experiments have suggested that this peptide may act in synergy with ACTH to increase corticosterone and aldosterone production in vivo and in vitro [30].
  • Whereas aldosterone is normally a much stronger mineralocorticoid than cortisol in vivo, mineralocorticoid receptors have identical in vitro affinities for these hormones [31].
  • In metabolic balance studies, amiloride reversed thiazide-induced urinary potassium loss, restored plasma bicarbonate concentration and pH to pretreatment levels, and produced further increases in aldosterone secretion [32].

Gene context of ALDOSTERONE

  • Expression studies demonstrate its ability to bind aldosterone with high affinity and to activate gene transcription in response to aldosterone, thus establishing its identity as the human mineralocorticoid receptor (hMR) [33].
  • Although two different ET-1 receptors have been identified and cloned, the receptor subtype involved in mediating aldosterone secretion is still unknown [34].
  • The enzyme 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD2) is selectively expressed in aldosterone target tissues, where it confers aldosterone selectivity for the mineralocorticoid receptor by inactivating 11 beta-hydroxyglucocorticoids [35].
  • CFTR has been proposed as a regulator of the 30 pS, ATP-sensitive renal K channel (Kir1.1, also known as renal outer medullar K [ROMK]) that is critical for K secretion by cells of the thick ascending limb (TAL) and distal nephron segments responsive to aldosterone [36].
  • Thus, in patients with congenital deficiency of 11 beta-HSD (the syndrome of apparent mineralocorticoid excess, AME), cortisol and not aldosterone acts as a mineralocorticoid, resulting in hypertension and hypokalaemia with suppression of the renin-angiotensin-aldosterone axis [37].

Analytical, diagnostic and therapeutic context of ALDOSTERONE

  • Two patients underwent intravenous infusion of [3H]progesterone for the measurement of extraadrenal production of 21-hydroxylated precursors of aldosterone [15].
  • The patient who had discontinued her medication excreted a normal amount of aldosterone (20.0 nmol per square meter of body-surface area per day) while following a diet low in sodium [15].
  • Radioimmunoassay revealed that the low dose of aldosterone restored plasma aldosterone to control levels [38].
  • We conclude that adrenalectomy impairs reabsorptive NaCl but not K transport in the Mtal, and that aldosterone restores this process [39].
  • Na-K-ATPase activity was measured with an ultramicromethod in single portions of the proximal and distal convolution and of the thick ascending limb of Henle from adrenalectomized rats and after treatment with 5 mug aldosterone per 100 g body wt [40].


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