title: When is cortisol a mineralocorticoid?
abstract: (1) Decreased 11 beta-OHSD activity permits binding of cortisol to the Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid excess (AME). (2) Blockade of either the Type I receptor with spironolactone or the Type II (glucocorticoid) receptor with RU-486 does not consistently abolish the effects of stress level cortisol on Na+ retention and hypertension in acute studies in normal humans, suggesting the existence of an additional glucocorticoid receptor. (3) Enhanced glucocorticoid 6 beta-hydroxylation could play an etiologic role in certain hypertensive syndromes. (4) Both decreased 11 beta-OHSD and increased 6 beta-OHase are candidates as intermediate phenotypes for the remote phenotype essential hypertension.
authors: J
authors: J
authors: Clore
authors: A
authors: A
authors: Schoolwerth
authors: C O
authors: CO
authors: Watlington
mesh_terms: D042842:11-beta-Hydroxysteroid Dehydrogenases; D000818:Animals; D005938:Glucocorticoids / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000502:physiology*; D006913:Hydroxysteroid Dehydrogenases / Q000172:deficiency; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology; D008901:Mineralocorticoids / Q000502:physiology*; D011965:Receptors, Glucocorticoid / Q000502:physiology
chemical_list: D005938:Glucocorticoids; D008901:Mineralocorticoids; D011965:Receptors, Glucocorticoid; D006913:Hydroxysteroid Dehydrogenases; D042842:11-beta-Hydroxysteroid Dehydrogenases; D006854:Hydrocortisone