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The influence of niflumic acid (3 and 10 microM), a Cl- channel antagonist, on cirazoline-induced
vasoconstriction in isolated perfused mesenteric artery (5 ml/min) from two-kidney
one-clip (2K1C) hypertensive and sham normotensive rats was examined. In addition,
the effect of a single i.v. bolus injection of niflumic acid (3 mg/kg) on cirazoline-mediated
reduction in vascular conductance in superior mesenteric artery was determined in
pentobarbital-anaesthetized hypertensive and normotensive rats. Bolus injections of
cirazoline induced a dose-dependent transient increase in the perfusion pressure in
vitro. In the presence of niflumic acid, cirazoline-mediated vasoconstriction was
significantly inhibited. Cirazoline-induced vasoconstriction in isolated mesenteric
beds was also significantly inhibited following perfusion with Cl(-)-free buffer.
Pre-perfusion of mesenteric blood vessels with Cl(-)-free buffer resulted in a significantly
greater inhibition of cirazoline-mediated vasoconstriction in sham normotensive rats
than in hypertensive rats. We found that in Cl(-)-free buffer, cirazoline-mediated
vasoconstriction could be further inhibited by niflumic acid. Intravenous infusion
of cumulative doses of cirazoline in vivo caused a dose-dependent decrease in superior
mesenteric vascular conductance. Pretreatment with niflumic acid significantly impaired
cirazoline-mediated decreases in vascular conductance. Our results indicate that chloride
ions play an important role in alpha1-adrenoceptor-mediated vasoconstriction in mesenteric
blood vessels. In addition, the contribution of chloride ions in alpha1-adrenoceptor-mediated
vasoconstriction in blood vessels from hypertensive rats appears to be reduced.