Abstract

Renin secretion is inversely related to afferent arteriolar transmural pressure, or to some function of it such as stretch (the baroreceptor mechanism). It has been suggested that increased pressure depolarizes the renin-secreting juxtaglomerular cells, and that increased Ca influx through voltage-operated Ca channels mediates the inhibitory effect on renin secretion. If true, then Ca channel blockers should antagonize the inhibitory effect of increased pressure on renin secretion. To test this prediction, isolated rat kidneys were perfused with an oxygenated physiological salt solution in a single-pass system. Perfusate flow rate and renin concentration in the venous effluent were measured and their product, the renin secretory rate (RSR), was calculated. During the control period, increasing renal perfusion pressure (RPP) from 100 to 120 mm Hg decreased RSR to 42 +/- 5% of the control value. This inhibitory effect of increased RPP was blunted by 1 microM nifedipine, nearly blocked by 5 microM verapamil and completely blocked by 50 microM diltiazem. Inasmuch as nifedipine, verapamil and diltiazem are Ca channel blockers and because all three have been shown previously to block the inhibitory effect of depolarization on RSR, these results are consistent with the hypothesis that a depolarization-induced influx of Ca mediates the inhibitory effect of increased RPP on RSR.