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 > α,β-methyleneATP > adenosine tetraphosphate ≥ β,γ-methyleneATP ≥ ATP = UTP ⪢ adenosine. Suramin (100 μM) blocked the contractile effects of 2-methylthioATP and α,β-methyleneATP, but not those of ATP and adenosine tetraphosphate. The P 1 purinoceptor antagonist, 8-phenyltheophylline (10 μM), 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 172 C58 (4-benzoyl-xylocholine, 10 μM), but not by suramin. α,β-MethyleneATP was more potent than β,γ-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 P 2 purinoceptors; these include a P 2x subtype, mediating contraction.

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