Abstract
Our study aimed to assess a possible functional role of the Na(+)/Ca(2+) exchanger in the regulation of renal vascular resistance (RVR). Therefore, we investigated the effects of an inhibition of the Na(+)/Ca(2+) exchanger either by lowering the extracellular sodium concentration ([Na(+)](e)) or, pharmacologically on RVR, by using isolated perfused rat kidneys. Graded decreases in [Na(+)](e) led ...
Abstract
Our study aimed to assess a possible functional role of the Na(+)/Ca(2+) exchanger in the regulation of renal vascular resistance (RVR). Therefore, we investigated the effects of an inhibition of the Na(+)/Ca(2+) exchanger either by lowering the extracellular sodium concentration ([Na(+)](e)) or, pharmacologically on RVR, by using isolated perfused rat kidneys. Graded decreases in [Na(+)](e) led to dose-dependent increases in RVR to 4.3-fold (35 mM Na(+)). This vasoconstriction was markedly attenuated by lowering the extracellular calcium concentration, by the L-type calcium channel blocker amlodipine or by the chloride channel blocker niflumic acid. Further lowering of [Na(+)](e) to 7 mM led to an increase in RVR to 7.5-fold. In this setting, amlodipine did not influence the magnitude but did influence the velocity of vasoconstriction. Pharmacological blockade of the Na(+)/Ca(2+) exchanger with KB-R7943, benzamil, or nickel resulted in significant vasoconstriction (RVR 2.5-, 1.8-, and 4.2-fold of control, respectively). Our data suggest a functional role of the Na(+)/Ca(2+) exchanger in the renal vascular bed. In conditions of partial replacement of [Na(+)](e), vasoconstriction is dependent on chloride and L-type calcium channels. A total replacement of [Na(+)](e) leads to a vasoconstriction that is nearly independent of L-type calcium channels. This might be due to an active calcium transport into the cell by the Na(+)/Ca(2+) exchanger.
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