Blockade of ATP-Sensitive Potassium Channels in Cerebral Arterioles Inhibits Vasoconstriction From Hypocapnic Alkalosis in Cats

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Abstract
Background and Purpose —Recent studies have shown that the cerebral arteriolar dilation from hypercapnic acidosis is blocked by agents which inhibit K ATP channels. These findings suggested that this response is due to opening of K ATP channels. Because the repose to CO 2 is a continuum, with hypercapnic acidosis causing vasodilation and hypocapnic alkalosis causing vasoconstriction, it would be expected that the response to hypocapnic alkalosis would be due to closing of K ATP channels. There are no studies of the effect of inhibition of K ATP channels on the response to hypocapnic alkalosis. Methods —We investigated the effect of 3 agents that in earlier studies were found to inhibit K ATP channels— N G -nitro- l -arginine, hydroxylysine, and glyburide—on the cerebral arteriolar constriction caused by graded hypocapnia induced by hyperventilation in anesthetized cats equipped with cranial windows. Results —Hypocapnic alkalosis caused dose-dependent vasoconstriction that was inhibited completely by each of the 3 inhibitors of K ATP channels. The blockade induced by these agents was eliminated in the presence of topical l -lysine (5 μmol/L). Conclusions —The findings show that agents which inhibit ATP-sensitive potassium channels in cerebral arterioles inhibit the vasoconstriction from hypocapnic alkalosis. These and earlier results showing that inhibition of K ATP channels inhibited dilation from hypercapnic acidosis demonstrate that the response to CO 2 in cerebral arterioles is mediated by the opening and closing of K ATP channels.