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Key reproductive events, such as menstruation and implantation, are considered to be inflammatory processes and glucocorticoids act as anti-inflammatory agents. The balance of expression of types 1 and 2 11β-hydroxysteroid dehydrogenases (11βHSD) controls the availability of cortisol to bind to the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR). Expression profiles of glucocorticoid-metabolising...
The 11β-hydroxysteroid dehydrogenase (11β-HSD) enzymes convert corticosterone and cortisol to 11-dehydrocorticosterone and cortisone, and are thought to convey extrinsic specificity to the mineralocorticoid receptor by limiting access of the relatively more abundant glucocorticoids to it. Two different 11β-hydroxysteroid dehydrogenases (11β-HSD) have been described and cloned. The liver-type, NADP...
Patients with ectopic ACTH syndrome often develop hypertension and hypokalemic alkalosis with an abnormal increase in the ratio of plasma cortisol to cortisone, indicating that 11β-hydroxysteroid dehydrogenase (11βHSD) activity is inhibited. Inhibition of 11βHSD allows access of cortisol or corticosterone to the mineralocorticoid receptor where it act as a mineralocorticoid. Two isozymes, 11βHSD-1...
Mineralocorticoid receptor (MR) selectivity for aldosterone is thought to be exerted by enzymes which inactivate competing glucocorticoids before they bind the receptor. Two different 11β-hydroxysteroid dehydrogenases (11β-HSD) have been described. 11β-HSD-1 is NADP + -dependent and has a K m in the micromolar range and bidirectional activity. 11β-HSD-2 is NAD + -dependent,...
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