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The effects of sodium nitroprusside on the electrical and mechanical properties of the guinea-pig vas deferens were studied and compared with those on the portal vein and the taenia coli. Sodium nitroprusside at concentrations higher than 0.5 mM caused depolarization of the membrane of the vas deferens and initiated spontaneous contractions, while spontaneous contractions of the portal vein were blocked by similar concentration of the drug. Noradrenaline- and carbachol-induced contractions of the vas deferens were markedly potentiated by sodium nitroprusside, whereas the noradrenaline-induced contraction of the portal vein was suppressed by the same concentration of the drug. Increasing the K+ concentration by 15 to 30 mM caused a similar potentiation of the contraction by noradrenaline or carbachol in the vas deferens. When sodium nitroprusside was applied during the course of noradrenaline- or carbachol-induced contracture, contraction was observed in the vas deferens, while relaxation was induced in the portal vein and taenia coli. In either case, however, the addition of Ca caused a relaxation of the preparations. These results suggest that the membrane depolarization may be involved in the stimulating effects sodium nitroprusside in the guinea-pig vas deferens.

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Stimulating and potentiating effects of sodium nitroprusside on the guinea-pig vas deferens and their comparison with the effects on the portal vein and the taenia coli.