Abstract
UTP, ATP and several of its analogues enhanced contractions of the longitudinal smooth muscle layer of the guinea-pig portal vein. The rank order of potency was 2-methylthioATP > alpha, beta-methyleneATP > adenosine tetraphosphate > or = beta, gamma-methyleneATP > or = ATP = UTP > > adenosine. Suramin (100 microM) blocked the contractile effects of 2-methylthioATP and alpha,beta-methyleneATP, but not those of ATP and adenosine tetraphosphate. The P1 purinoceptor antagonist, 8-phenyltheophylline (10 microM), was without effect on the response to ATP. Field stimulation (5 s trains every 100 s, 1 ms, 55 V) caused frequency-dependent contractions that were partially reduced by the noradrenergic neurone blocking drug; BW 172C58 (4-benzoyl-xylocholine, 10 microM), but not by suramin. alpha,beta-MethyleneATP was more potent than beta,gamma-methyleneATP, UTP and adenosine tetraphosphate in partially inhibiting field stimulation-induced contractions of the portal vein; its effects, but not those of adenosine tetraphosphate, were reduced by suramin. These results indicate that the guinea-pig portal vein contains P2 purinoceptors; these include a P2x subtype, mediating contraction.
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