Corticosteroid 11-beta-dehydrogenase isozyme 2Cortisol and test finale primo soccorso aziendale have the same in vitro affinity for the mineralocorticoid receptor MRalthough in vivo only aldosterone acts as a physiologic agonist of the MR, despite circulating levels of cortisol in humans and corticosterone in rodents being three orders of magnitude higher than aldosterone levels. The gene is highly expressed in all sodium-transporting epithelia, particularly in the kidney and colon, but also in human placenta and vascular wall. These abnormalities may 11 beta hydroxysteroid dehydrogenase type 2 deficiency genetically determined, as suggested by the association of a microsatellite flanking the HSD11B2 gene with hypertension in black patients with end-stage kidney disease and with salt sensitivity of blood pressure in healthy subjects. These findings indicate that variants of the HSD11B2 gene may contribute to the enhanced blood pressure response to salt dehysrogenase possibly to hypertension in humans. Author links open overlay panel 11 beta hydroxysteroid dehydrogenase type 2 deficiency Ferrari. Under an Elsevier user license. Abstract Cortisol bega aldosterone have the same in vitro affinity for the mineralocorticoid receptor MRalthough in vivo only aldosterone acts as a physiologic agonist of the MR, despite circulating levels of cortisol in humans and corticosterone in rodents being three orders of magnitude higher than aldosterone levels.
11β-Hydroxysteroid dehydrogenase - Wikipedia
HSDB2 expression is also found in the brainstem in a small, aldosterone-sensitive subset of neurons located in the nucleus of the solitary tract referred to as HSD2 neurons.
In these tissues, HSD11B2 oxidizes the glucocorticoid cortisol to the inactive metabolite cortisone , thus preventing illicit activation of the mineralocorticoid receptor.
This protective mechanism is necessary because cortisol circulates at fold higher concentrations than aldosterone, and binds with equal affinity to the mineralocorticoid receptor, thereby out-competing aldosterone in cells that do not produce HSD11B2. This glucocorticoid-inactivating enzyme is also expressed in tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, as well as parts of the developing brain, including the rhombencephalic progenitor cells that proliferate into cerebellar granule cells.
Inhibition of this enzyme, for example by a compound in liquorice, results in a condition known as pseudohyperaldosteronism. A genetically inherited deficiency of HSD11B2 is the underlying cause of the syndrome of apparent mineralocorticoid excess. From Wikipedia, the free encyclopedia. Chromosome 16 human . HSD11B2 hydroxysteroid beta dehydrogenase 2". American Journal of Physiology.
Quinkler M, Stewart PM Mevalonate kinase Phosphomevalonate kinase Pyrophosphomevalonate decarboxylase Isopentenyl-diphosphate delta isomerase. Farnesyl-diphosphate farnesyltransferase Squalene monooxygenase Lanosterol synthase. D-lactate dehydrogenase cytochrome D-lactate dehydrogenase cytochrome c Mannitol dehydrogenase cytochrome. Glucose oxidase L-gulonolactone oxidase Xanthine oxidase. Vitamin K epoxide reductase Vitamin-K-epoxide reductase warfarin-insensitive. Malate dehydrogenase quinone Quinoprotein glucose dehydrogenase.
Allosteric regulation Cooperativity Enzyme inhibitor. EC number Enzyme superfamily Enzyme family List of enzymes. Molecular and Cellular Biology portal. Retrieved from " https: Genes on human chromosome 16 EC 1. Views Read Edit View history.