Methanol-induced contraction of canine cerebral artery and its possible mechanism of action

Toxicology and Applied Pharmacology
W LiB M Altura

Abstract

In the present report, we investigated the effects of methanol on canine basilar cerebral arterial rings. Our data indicate that acute methanol exposure (5-675 mM) induces potent contractile responses of cerebral arteries in a concentration-dependent manner. Pharmacological antagonists, such as propranolol, phentolamine, haloperidol, methysergide, naloxone, diphenhydramine, and cimetidine, did not exert any effects on these methanol-induced contractions. Likewise, a potent antagonist of cyclo-oxygenase, and subsequent synthesis of prostanoids (i.e., indomethacin), failed to exert any effect on methanol-induced contractions. No differences in responsiveness to methanol in canine cerebral arteries were found in vessel segments with or without endothelial cells. Removal of extracellular Ca2+ ([Ca2+]o) partially attenuated methanol-induced contractions, while withdrawal of extracellular Mg2+ ([Mg2+]o) potentiated the contractions. In the complete absence of [Ca2+]o, 10 mM caffeine and 400 mM methanol induced similar, transient contractions followed by relaxation in K(+)-depolarized cerebral vascular tissues. Methanol-induced contractions were, however, completely abolished by pretreatment of tissue with 10 mM caffeine. Our results ...Continue Reading

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