RT Journal Article
SR Electronic
T1 Role of calcium in the interaction of alpha and beta adrenoceptor-mediated renin release in isolated, constant pressure perfused rabbit kidneys.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 144
OP 149
VO 227
IS 1
A1 T J Opgenorth
A1 J E Zehr
YR 1983
UL http://jpet.aspetjournals.org/content/227/1/144.abstract
AB These experiments were designed to study the role of calcium in the modulation of renin secretion by alpha and beta adrenoceptors. Rabbit kidneys were isolated and single-pass perfused with a modified Ringer's solution. Renal perfusion pressure was precisely controlled by an electronic servocontrol system. Tubular events were minimized by ligation of the ureter before initiating the studies. Under these conditions the predominant factor modifying renin secretion was assumed to originate directly on the juxtaglomerular cells. Isoproterenol infused at 0.1, 0.5, 1.0 and 5.0 nM/min/g of kidney weight increased renin secretion in a dose-dependent manner whereas phenylephrine infused at identical molar doses did not. In addition, phenylephrine (5.0 nM/min/g of kidney weight) blocked the usual response to isoproterenol. Removal of calcium from the perfusing medium had no effect on either the response to isoproterenol or the lack of a response to phenylephrine. On the other hand, when calcium is removed from the perfusate or when D-600, a calcium channel blocker, is added to calcium-containing medium, phenylephrine failed to block the usual response to isoproterenol. We conclude that the suppression of beta adrenoceptor stimulation of renin release by alpha adrenoceptor agonists is calcium dependent by a final mechanism as yet undefined, but probably involving movement of calcium into the juxtaglomerular cells.