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

Academic Article

Abstract

  • 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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    Keywords

  • Animals, Arterioles, Calcium, Female, In Vitro Techniques, Kidney Glomerulus, Kinetics, Membrane Potentials, Muscle, Smooth, Vascular, Nifedipine, Potassium, Rabbits, Renal Circulation, Time Factors
  • Digital Object Identifier (doi)

    Authorlist

  • Carmines PK; Fowler BC; Bell PD
  • Start Page

  • F677
  • End Page

  • F685
  • Volume

  • 265
  • Issue

  • 5 Pt 2