The Role of the Adrenal Glands in Sodium Excretion Evoked by Centrally Administered Renin 1

Abstract

Abstract

Renin or angiotensin, when administered into the central nervous system, increases urinary sodium excretion but the mechanism is undefined. In addition, central angiotensin injections reduce plasma aldosterone concentration. Thus, diminished mineralocorticoid effects on the kidneys may explain the natriuresis. This hypothesis was tested by intracerebroventricular (IVT) renin injections (5 mGU/5 μl) in conscious, hydrated rats pretreated 90 min beforehand with d-aldosterone (20 μg/kg ip). Aldosterone did not affect renin-induced sodium output at 3 and 6 hr, although it reduced the Na/K ratio at 3 hr. Other rats were sham-operated or bilaterally adrenalectomized. Four days later, they were pretreated with aldosterone and given an oral water load followed by IVT renin or saline. Basal sodium excretion in adrenalectomized rats was reduced; natriuresis after renin was still evident but of reduced magnitude compared to sham rats. Although IVT renin and angiotensin lower the plasma aldosterone concentration, the natriuretic effect of IVT renin is independent of mineralocorticoids. Likewise, natriuresis can occur in the absence of the adrenal glands, although the magnitude is reduced.