Corticosteroid hypertension.
Over the past year, the focus in corticosteroid hypertension has been on the cloning of the enzyme 11 beta-hydroxysteroid dehydrogenase, and the demonstration of a variety of mutations or deletions in the sequence coding for this enzyme in the syndrome of apparent mineralocorticoid excess. This syndrome is the third single-gene cause of human hypertension to be characterized, with glucocorticoid remediable aldosteronism (1992) and Liddle's syndrome (1994). The three conditions are characterized by inappropriate control of aldosterone secretion (glucocorticoid remediable aldosteronism), sodium retention (Liddle's syndrome) or aldosterone action (apparent mineralocorticoid excess), and underline a potential role of an aldosterone: salt imbalance in mineralocorticoid hypertension. No comparable mechanisms of hypertension following glucocorticoid receptor occupancy have been documented to date.
Funder
J W
JW
Baker Medical Research Institute, Prahran, Victoria, Australia.
D000305:Adrenal Cortex Hormones / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D009154:Mutation; D011987:Receptors, Steroid / Q000235:genetics / Q000378:metabolism*
D000305:Adrenal Cortex Hormones; D011987:Receptors, Steroid