Control of renin secretion in the anesthetized dog

Renin concentrations of renal venous plasma were indirectly measured by bio-assaying the pressor activity produced by plasma incubation under standardized conditions. Pressor activity was detectable in 85% of control dogs, was reciprocally related to sodium excretion, but did not correlate with arterial blood pressure. Reduction of mean renal arterial pressure to 90 mm Hg by an aortic clamp decreased sodium excretion and produced sustained increases in renin secretion and arterial blood pressure proximal to the clamp. Release of the aortic clamp resulted in gradual return of these variables toward control values. Induction of diuresis (osmotic diuretics, chlorothiazide, or acetazolamide) prior to aortic clamping minimized or completely prevented the usual clamp-induced rises in renin secretion and proximal blood pressure. Induction of diuresis during aortic clamping returned the elevated renin secretion and proximal blood pressure toward control values. These effects of diuretics could not be explained by changes in renal hemodynamics or plasma composition. Elevation of ureteral pressure in nondiuretic dogs also increased renin secretion and arterial blood pressure. We conclude that renin secretion is not controlled by blood pressure, per se, or intrarenal pressure, but by the flow or composition of intratubular fluid, probably at the level of the macula densa.