Abstract
Experiments were performed to determine the effect of a chloride channel blocker (indanyloxyacetic acid, IAA-94) on renal arteriolar vasoconstrictor responses to angiotensin II (AngII). The in vitro blood-perfused juxtamedullary nephron technique was exploited to provide access to the renal microvasculature of enalaprilat-treated rats. Under control conditions, 1 to 100 nmol/L AngII evoked concentration-dependent afferent arteriolar vasoconstriction. Baseline diameter of afferent arterioles was not altered by 30 mumol/L IAA-94; however, AngII responsiveness was markedly attenuated. The afferent response to K-induced depolarization was sustained in the presence of IAA-94. In efferent arterioles, neither baseline diameter nor AngII responsiveness was altered by IAA-94. These results suggest that full expression AngII-induced afferent (but not efferent) arteriolar vasoconstriction requires participation of chloride channels, which likely engender depolarization and subsequent opening of voltage-gated calcium channels.
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