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.