Abstract
Summary
In anesthetized salt-depleted dogs, renal venous renin activity correlated directly with renal vascular resistance and inversely with RPF, but not with arterial blood pressure, GFR, filtration fraction, urine flow, or sodium excretion. Acetylcholine, 50–100 μg/min, infused directly into a renal artery caused significant vasodilation and natriuresis, but no significant, change in renal venous renin for the group as a whole. However, definite inhibition of renin release was observed in the 3 dogs with the highest control renal resistance. For the entire group, cessation of acetylcholine infusion was followed by a transient significant increase of renin above the initial control value. The data do not support the hypothesis that vasoconstriction is the major stimulus to renin release during salt depletion, but do not rule it out because of the possibility that acetylcholine might induce simultaneous opposing effects, one inhibiting and the other stimulating renin release.
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