Angiotensin II and K challenge following prolonged ACTH administration to normal subjects.
Twelve healthy male volunteers on a normal Na and K intake and ambulatory received ACTH (40 IU, im) twice daily for 5 days followed by 2 days of angiotensin II (5--13 ng/kg body weight/min for 60 min) or oral K citrate (30 mEq./h x 3). A discordance in the aldosterone-stimulating and pressor responses of angiotensin II was unmasked with only the latter response being positive following ACTH-induced refractoriness. K loading was a much more potent natriuretic stimulus than angiotensin II treatment. In contrast to angiotensin II, K could selectively enhance aldosterone secretion by overcoming the inhibition in secretion of the mineralocorticoid induced by prolonged ACTH exposure.
D000284:Administration, Oral; D000324:Adrenocorticotropic Hormone / Q000008:administration & dosage / Q000494:pharmacology*; D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D007263:Infusions, Parenteral; D008297:Male; D011188:Potassium / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism
D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D011188:Potassium; D006854:Hydrocortisone