SEGMENT-SPECIFIC EFFECT OF CHLORIDE CHANNEL BLOCKADE ON RAT RENAL ARTERIOLAR CONTRACTILE RESPONSES TO ANGIOTENSIN-II

Experiments were performed to determine the effect of a chloride chann el blocker (indanyloxyacetic acid, IAA-94) on renal arteriolar vasocon strictor responses to angiotensin II (AngII). The in vitro blood-perfu sed juxtamedullary nephron technique was exploited to provide access t o the renal microvasculature of enalaprilat-treated rats. Under contro l conditions, 1 to 100 nmol/L AngII evoked concentration-dependent aff erent arteriolar vasoconstriction. Baseline diameter of afferent arter ioles was not altered by 30 mu mol/L IAA-94; however, AngII responsive ness was markedly attenuated. The afferent response to K-induced depol arization was sustained in the presence of IAA-94. In efferent arterio les, neither baseline diameter nor AngII responsiveness was altered by IAA-94. These results suggest that full expression AngII-induced affe rent (but not efferent) arteriolar vasoconstriction requires participa tion of chloride channels, which likely engender depolarization and su bsequent opening of voltage-gated calcium channels.