Calcium in neural control of renal circulation.

We assessed the role of calcium in neurogenically mediated alterations of the renal circulation in the isolated perfused rat kidney. The transarterial application of high-frequency renal nerve stimulation (RNS) increased renal vascular resistance (RVR) by 50% (P less than 0.001). Concomitantly, glomerular filtration rate (GFR), urine flow (V), and sodium excretion (UNaV) decreased by 83, 82, and 78%, respectively (P less than 0.006 for all). Kidneys obtained from rats that had undergone prior chemical sympathectomy by 6-hydroxydopamine treatment did not respond to RNS. Addition of the calcium channel-blocking agents, verapamil or diltiazem (5 microM), during RNS of normal kidneys completely reversed the changes in GFR, V, and UNaV and returned RVR nearly to control. Aside from a small decrease in RVR and an increase in V produced by verapamil, diltiazem or verapamil alone did not affect kidney function. Norepinephrine (5-8 microM) increased RVR 50% and decreased GFR, V, and UNaV similarly to RNS. When added to perfusate in the presence of norepinephrine, verapamil reversed all these changes. With a low-calcium perfusate (0.4 mM total calcium), RNS did not increase RVR and did not decrease GFR, V, or UNaV. These results indicate that the circulatory changes produced in the isolated rat kidney by high-frequency RNS depend critically upon the extracellular calcium, are closely reproduced by norepinephrine, and are largely reversed by calcium channel blockers.