The role of calcium in the control of renin release from the isolated rat kidney.

Abstract

The effect of verapamil and manganese on isoproterenol- and glucagon-evoked renin secretion and on norepinephrine-induced renal vasoconstriction was studied in the isolated perfused kidney. Results for renin secretion and perfusate flow rates were expressed as the ratio of the average of the two values which deviated furthest from base line during the experimental period to the average of two control values determined at the beginning of each experiment. Norepinephrine significantly reduced (p < 0.001) the perfusate flow ratio to 0.35 ± 0.06 (mean ± SEM) without having any effect on renin secretion. During Ca2+-free perfusion, norepinephrine-induced renal vasoconstriction was completely abolished and concomitantly the renin secretion ratio increased significantly (p < 0.001) to 6.28 ± 1.24. Verapamil attenuated and manganese chloride abolished norepinephrine-induced renal vasoconstriction. Renin secretion increased significantly (p < 0.001) to 9.26 ± 1.79 and 9.92 ± 1.93 in the verapamil and manganese experiments, respectively. Verapamil and manganese themselves did not significantly alter renin secretion or perfusate flow and neither inhibited renin secretion induced by isoproterenol and glucagon. In conclusion, extracellular Ca2+ and net Ca2+ influx are prerequisites for norepinephrine to produce renal vasoconstriction and to inhibit renin release in the isolated perfused kidney. On the other hand, renin secretion evoked by isoproterenol and glucagon does not seem to require the movement of extracellular calcium into juxtaglomerular cells and it is speculated that the level of adenylate cyclase activity may be an important determinant of the rate of renin release.