Primacy of the renin-angiotensin system in mediating the aldosterone response to sodium restriction.

The primacy of angiotensin II as the mediator of the adrenal's response to sodium restriction is controversial. We administered the oral converting enzyme inhibitor, captopril (SQ 14225), to test whether reduction of angiotension II generation for 26 h in sodium-restricted subjects would lower plasma aldosterone levels to values observed in subjects on a high sodium intake. Accordingly, plasma angiotensin II and aldosterone levels were measured in nine recumbent normal subjects on high (200 meq) and low (10 meq) sodium intakes and low sodium intake with captopril (12.5--25 mg four times a day for 26 h). Captopril reduced the sodium-restricted angiotensin II levels from 31 +/- 6 to 13 +/- 2 pg/ml, which was indistinguishable from that measured on the high sodium intake (11 +/- 2 pg/ml). Concomitantly, aldosterone levels were reduced from 25 +/- 4 to 7 +/- 1 ng/dl, which was similar to the high sodium value (8 +/- 1 ng/dl). There were no significant changes in serum sodium, cortisol, or potassium at the three sampling times. Thus, the complete suppression of the sodium-restricted levels of both angiotensin II and aldosterone into the high sodium range by captopril provides strong support for the hypothesis that the renin-angiotensin system is the prime mediator of the adrenal's response to sodium restriction.