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Stroke, Vol 14, 347-355, Copyright © 1983 by American Heart Association

ARTICLES

Mechanisms of the contractile effect induced by uridine 5-triphosphate in canine cerebral arteries

Y Shirasawa, RP White and JT Robertson

This study was performed to elucidate mechanisms responsible for the contraction of isolated canine cerebral arteries induced by uridine 5'- triphosphate (UTP) and to ascertain whether UTP given intracisternally causes cerebral arterial constriction. The latter was proven arteriographically to be the case. In vitro, UTP (10(-4)M) and UDP were similar in potency, produced sustained contractions, and were more effective than other pyrimidine nucleotides or uridine. Unlike serotonin (5-HT), UTP was not antagonized by cinanserin and failed to cause constriction of mesenteric arteries. Adenosine similarly antagonized 5-HT and UTP. The Ca2+ antagonist nimodipine abolished contractions caused by high K+ but only incompletely antagonized 5-HT or UTP. On the other hand, procedures that hyperpolarize the cell membrane (low K+ followed by K+) abolished tonic contractions induced by UTP. Hyperpolarization prior to UTP (with or without nimodipine) did not, however, prevent the occurrence of a phasic contraction. Papaverine or lanthanum antagonized this phasic response. It was concluded that UTP selectively affects cerebral arteries, may initiate contraction by releasing membrane bound Ca2+, depolarizes the cell membrane to open receptor operated and potential sensitive calcium channels, but does not inhibit the electrogenic Na-pump nor specifically antagonize the vasodilator adenosine.

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