Hypertension corrected and aldosterone responsiveness to renin-angiotensin restored by long-term dexamethasone in glucocorticoid-suppressible hyperaldosteronism.
Two males with glucocorticoid-suppressible hyperaldosteronism had hyperaldosteronism, hypertension and hypokalaemia corrected by continuous administration of physiological doses of dexamethasone for more than a year. During long-term dexamethasone treatment: (a) Plasma renin activity increased from subnormal to high normal levels, with normal posture-mediated increases; (b) Plasma aldosterone became responsive to angiotensin infusion, a new observation; (c) A fall in plasma aldosterone between 0800 h (recumbent) and 1000 h (upright) was replaced by a rise; (d) Plasma aldosterone became suppressible with salt loading. These findings are consistent with a shift to more normal control of aldosterone by renin-angiotensin, once abnormal responsiveness to ACTH has been nullified.
Woodland
E
E
Tunny
T J
TJ
Hamlet
S M
SM
Gordon
R D
RD
D000293:Adolescent; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000450:Aldosterone / Q000097:blood*; D000809:Angiotensins / Q000494:pharmacology*; D003907:Dexamethasone / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D006929:Hyperaldosteronism / Q000188:drug therapy / Q000378:metabolism*; D006973:Hypertension / Q000188:drug therapy; D008297:Male; D012083:Renin / Q000097:blood*
D000809:Angiotensins; D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D012083:Renin