Aldosterone response to hypoglycemia: evidence of ACTH mediation.
Insulin-induced hypoglycemia caused an increase in plasma aldosterone as well as in renin activity and cortisol. After the suppression of the renin-angiotensin system by the prior administration of propranolol, insulin-induced hypoglycemia still caused a significant increase in plasma aldosterone similar to the increase in plasma cortisol, though plasma renin activity was suppressed. Conversely, after the suppression of endogenous ACTH by the prior admininstration of dexamethasone, insulin-induced hypoglycemia failed to induce a rise in plasma aldosterone and plasma cortisol, through plasma renin activity increased. The increase of plasma aldosterone in response to exogenous ACTH was not different with or without the prior administration of dexamethasone. We conclude that ACTH is largely responsible for the increased aldosterone secretion after insulin-induced hypoglycemia.
D000324:Adrenocorticotropic Hormone / Q000502:physiology*; D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000097:blood; D003864:Depression, Chemical; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism
D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D011433:Propranolol; D012083:Renin; D011188:Potassium; D006854:Hydrocortisone