Aldosterone response to prolonged ACTH infusion in juvenile hypertension.
The effects of a continuous 5-day ACTH infusion (40 units/24 hr) on plasma aldosterone (aldo) concentration and urinary excretion of aldosterone pH 1 conjugate, tetrahydroaldosterone and free aldo were investigated in 6 normotensive children, and 7 children with hypertension of unknown origin. In both groups, an initial rise of plasma aldo and all urinary aldo metabolites and a subsequent fall were observed during the ACTH test. The decline in plasma aldo correlated significantly with a decrease in plasma renin activity and serum K+. There was, however, evidence for another regulatory factor of aldo secretion during ACTH infusion because on a low salt diet. ACTH produced a similar aldo pattern which could not be attributed to the changes in plasma renin activity or serum K+. Urinary excretion of both free aldo and tetrahydroaldosterone, a metabolite formed in the liver, showed a slower decrease during ACTH infusion than aldosterone pH 1 conjugate, which is of renal origin. The change in pattern of urinary aldo metabolites may be caused by a relative increase of the free, nonprotein bound plasma fraction of aldo and an enhanced metabolism of aldo in the liver during ACTH infusion. Neither in the baseline state nor during the ACTH test was there a difference between the normotensive and the hypertensive group in any of the aldo parameters.
D000293:Adolescent; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000450:Aldosterone / Q000378:metabolism*; D002648:Child; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism; D013997:Time Factors
D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D012083:Renin; D011188:Potassium