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

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 μM 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.