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 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.
Carmines
P K
PK
Department of Physiology & Biophysics, University of Nebraska Medical Center, Omaha 68198-4575, USA.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001160:Arterioles / Q000187:drug effects* / Q000503:physiopathology; D018118:Chloride Channels / Q000037:antagonists & inhibitors*; D006016:Glycolates / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects*
D018118:Chloride Channels; D006016:Glycolates; D000804:Angiotensin II; C015765:MK 473