SEGMENTALLY DISTINCT EFFECTS OF DEPOLARIZATION ON INTRACELLULAR [CA2+] IN RENAL ARTERIOLES

Experiments were performed to determine the influence of depolarizatio n on intracellular Ca2+ concentration ([Ca2+]i) in renal arterioles an d the possible role of voltage-gated Ca2+ channels in these responses. Glomeruli with attached arterioles and thick ascending limb were diss ected from rabbit kidney and loaded with fura 2. [Ca2+], of nonperfuse d arterioles was monitored using a microscope-based dual-excitation wa velength spectrofluorometry system. Afferent arteriolar (Ca2+]i averag ed 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 muM nifedipine, 100 mM K+ el icited a 10% decrease in afferent arteriolar [Ca2+]i (P < 0.05). Thus nifedipine reversed the afferent [Ca2+]i response to depolarization, i mplicating voltage-gated Ca2+ channels as the influx pathway. In contr ast to the behavior of afferent arterioles, the 100 mM K+ solution red uced 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 elicit ing depolarization-induced increases in afferent arteriolar [Ca2+]i wh ile failing to provide evidence for operation of such a mechanism at e fferent arteriolar sites.