Abstract
Synthetic arginine-vasopressin (ADH or antidiuretic hormone) inhibited renin secretory rate of rat renal cortical slices. The response was concentration-dependent and was maximal at 0.1 U ml-1. Ca depletion (incubation of slices in medium containing Na2EGTA [ethylene glycol bis (.beta.-aminoethyl ether) tetraacetate] and no added CaCl2) stimulated renin secretion and eventually abolished the inhibitory effect of ADH. Both effects were reversible. The Ca antagonist D-600 [methoxyverapamil] at 0.5 .mu.M, reversed the inhibitory effect of K depolarization on secretory rate but had no effect on secretory rate of non-depolarized slices. In the presence of 0.5 .mu.M-D-600, ADH inhibited the secretory rate of either depolarized or non-depolarized slices. These results confirm and extend previous observations suggesting that Ca plays an inhibitory coupling role in the control of renin secretion. They suggest that although Ca influx through voltage-sensitive Ca channels influences the secretory activity of juxtaglomerular cells, ADH activates an independent pathway for Ca mobilization.