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Am J Physiol Renal Physiol 265: F677-F685, 1993;
0363-6127/93 $5.00
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AJP - Renal Physiology, Vol 265, Issue 5 677-F685, Copyright © 1993 by American Physiological Society

ARTICLES

Segmentally distinct effects of depolarization on intracellular [Ca2+] in renal arterioles

P. K. Carmines, B. C. Fowler and P. D. Bell
Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112.

Experiments were performed to determine the influence of depolarization on intracellular Ca2+ concentration ([Ca2+]i) in renal arterioles and the possible role of voltage-gated Ca2+ channels in these responses. Glomeruli with attached arterioles and thick ascending limb were dissected from rabbit kidney and loaded with fura 2. [Ca2+]i of nonperfused arterioles was monitored using a microscope-based dual-excitation wavelength spectrofluorometry system. Afferent arteriolar [Ca2+]i averaged 150 +/- 11 nM (n = 20) when bathed in Ringer solution containing 1.5 mM Ca2+ and 5 mM K+. Replacement of the normal Ringer solution with one containing 100 mM K+ significantly increased afferent arteriolar [Ca2+]i to 196 +/- 12 nM. This response was abolished in the absence of extracellular Ca2+. In the presence of 1 microM nifedipine, 100 mM K+ elicited a 10% decrease in afferent arteriolar [Ca2+]i (P < 0.05). Thus nifedipine reversed the afferent [Ca2+]i response to depolarization, implicating voltage-gated Ca2+ channels as the influx pathway. In contrast to the behavior of afferent arterioles, the 100 mM K+ solution reduced efferent arteriolar [Ca2+]i from 188 +/- 17 to 148 +/- 13 nM (n = 11, P < 0.01), an effect that was not influenced by nifedipine. These observations support a role for voltage-gated Ca2+ channels in eliciting depolarization-induced increases in afferent arteriolar [Ca2+]i while failing to provide evidence for operation of such a mechanism at efferent arteriolar sites.


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