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The effects of sodium nitroprusside on potassium-induced phasic and tonic contraction of the guinea pig vas deferens and portal vein were studied. Sodium nitroprusside at concentrations higher than 10(-4) M potentiated the phasic contraction of potassium contracture of the vas deferens, while it showed no or slight depressing effect on the tonic contraction. Sodium nitroprusside at the same concentration depressed both the phasic and tonic contractions of the portal vein. Sodium nitroprusside depolarized the membrane of the vas deferens but did not alter the depolarization by K-Tyrode's solution. Potentiation of the phasic contraction was also observed following the pretreatment with 20 mM K+. When sodium nitroprusside was applied during the course of the tonic contraction, marked relaxation was observed in the portal vein, while only slight relaxation was induced in the vas deferens even by high concentrations of the drug. Residual tension in the presence of sodium nitroprusside was completely abolished by the application of verapamil of the concentration higher than 10(-6) M. Relaxations of preparation by sodium nitroprusside were counteracted by increases in Ca concentration. When sodium nitroprusside was applied in the presence of moderately elevated-K+ (15 to 30 mM), an increase in tension was observed in the vas deferens and a decrease in tension was observed in the portal vein. The differences in the action of sodium nitroprusside on the vas deferens and on the portal vein may be explained by the differences in the action of the drug on cell membrane, especially on the membrane potential.

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The effects of sodium nitroprusside on the phasic and tonic contraction of the potassium contractureof the smooth muscle of guinea-pig vas deferens and portal vein.