Studies on the mechanism by which ACTH stimulates renin activity and angiotensin II formation in man

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Abstract
Ten IU of ACTH (1-24) per day was infused for 34 h (starting at 0700 h) into 8 normal men on a constant diet containing 135 mM Na+/day. All subjects retained between 152 and 181 mM of Na. K balance was negative. Plasma renin activity (PRA) and plasma angiotension II (P-A II) started to rise in most subjects after 6-8 h of infusion, reached a maximum after 24 h and then tended to decline. As shown previously, the rise in PRA is not due to a rise in plasma renin substrate concentration. Systolic, but not diastolic blood pressure increased significantly on the 2nd day of ACTH infusion. Plasma cortisol (P-F) was continuously stimulated by ACTH. Plasma aldosterone (P-aldo) increased rapidly 1 h after ACTH administration, then tended to fall, and increased again in most subjects, roughly in parallel with PRA. No significant changes in electrolyte balance, PRA, P-A II, P-F and P-aldo occurred in 3 subjects receiving sham-infusions. Additional experiments in subjects treated with propranolol or indomethacin allowed the conclusion that the effect of ACTH on PRA and P-A II is not mediated by renal .beta.-adrenergic receptors, but perhaps (partially?) by prostaglandins. Since the infusion rate of ACTH was not much higher than the secretion rate of ACTH in early morning hours, it is possible that ACTH is physiologically involved in the regulation of renin secretion.