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L-type calcium channels in the renal microcirculatory response to endothelin

¹Vascular Biology Center and Departments of ²Surgery and ³Physiology, Medical College of Georgia, Augusta, Georgia

Submitted 19 August 2004 ; accepted in final form 11 November 2004

The signaling pathways of endothelin (ET)-1-mediated vasoconstriction in the renal circulation have not been elucidated but appear to be distinct between ET_A and ET_B receptors. The purpose of this study was to determine the role of L-type Ca²⁺ channels in the vasoconstrictor response to ET-1 and the ET_B receptor agonist sarafotoxin 6c (S6c) in the rat kidney. Renal blood flow (RBF) was measured with an ultrasonic flow probe in anesthetized rats, and a microcatheter was inserted into the renal artery for drug infusion. All rats were given vehicle (0.9% NaCl) or three successive bolus injections (1, 10, and 100 pmol) of ET-1 or S6c at 30-min intervals (n = 6 in each group). ET-1 and S6c produced dose-dependent decreases in RBF. The Ca²⁺ channel blocker nifedipine (1.5 µg) significantly attenuated the RBF response only at the highest doses of ET-1 and S6c. In the isolated blood-perfused juxtamedullary nephron preparation, Ca²⁺ channel blockade with diltiazem had a very small inhibitory effect on ET-1-induced decreases in afferent arteriolar diameter only at the lowest concentrations of ET-1. In vascular smooth muscle cells isolated from preglomerular vessels, ET-1 produced a typical biphasic Ca²⁺ response, whereas S6c had no effect on cytosolic Ca²⁺. Furthermore, Ca²⁺ channel blockade (diltiazem or Ni²⁺) had no effect on the peak or sustained increase in cytosolic Ca²⁺ produced by ET-1. These results support the hypothesis that L-type Ca²⁺ channels play only a minor role in the constrictor responses to ET-1 in the renal microcirculation.

renal blood flow; endothelin receptors; afferent arteriole; calcium channel blockers

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