Role of Intracellular Calcium in Renal Nerve-Mediated Renin Release

Abstract

Abstract

We evaluated the role of intracellular calcium in renal nerve-mediated renin release in four groups of anesthetized dogs. Each dog received renal nerve stimulation (RNS) (0.5 Hz) twice as follow: control, RNS, recovery; control, RNS, recovery. Group 1 served as time control. Group 2 received Ca ionophore A23187 (Io) and Groups 3 and 4 received verapamil at 2.5 and 5 μg/kg · min respectively during the second RNS. In Group 1, renin secretion rate (RSR) increased from 95 ± 22 to 223 ± 73 (P < 0.05) and from 13 ± 5 to 108 ± 20 ngANG I/hr · min (P < 0.005) during the first and second RNS, respectively. In Group 2, RSR increased from 210 ± 85 to 402 ± 118 (P < 0.02) and from 88 ± 11 to 157 ± 39 ngANG I/hr · min (NS) during the first and second RNS, respectively. In both groups, systemic and renal hemodynamics and UNaV did not change. In Group 3, verapamil alone did not increase RSR. During RNS, RSR also did not increase. In Group 4, verapamil alone increased RSR from 42 ± 12 to 273 ± 71 ngANG 1/hr · min (P < 0.03) despite a similar reduction in systemic blood pressure as in Group 3. RNS did not increase RSR further during verapamil infusion. The present study suggests that increased intracellular Ca by Io inhibits renal nerve-mediated renin release. A low dose of verapamil has no effect on renin release and does not augment renal nerve-mediated renin release. A high dose of veparamil increases renin release but does not enhance RNS-mediated renin release. We conclude that intracellular calcium plays an important role in renin release and may be the final messenger in renal nerve-mediated renin release.