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Am J Physiol Renal Physiol 280: F155-F161, 2001;
0363-6127/01 $5.00
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Vol. 280, Issue 1, F155-F161, January 2001

Functional role of sodium-calcium exchange in the regulation of renal vascular resistance

Frank Schweda1, Helga Seebauer1, Bernhard K. Krämer2, and Armin Kurtz1

1 Institut für Physiologie I and 2 Klinik und Poliklinik für Innere Medizin II, Universität Regensburg, D-93040 Regensburg, Germany

Our study aimed to assess a possible functional role of the Na+/Ca2+ exchanger in the regulation of renal vascular resistance (RVR). Therefore, we investigated the effects of an inhibition of the Na+/Ca2+ 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+/Ca2+ 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+/Ca2+ 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+/Ca2+ exchanger.

vasoconstriction; benzamil; KB-R7943; nickel


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