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PubMed1987

Comparison of agonistic and antagonistic actions of guanabenz and guanfacin on alpha 1 and alpha 2-adrenoceptors in isolated smooth muscles.

The effects of guanabenz, guanfacine and clonidine on alpha-adrenoceptors were investigated in isolated rat vas deferens and rabbit aortic strip. All 3 drugs at low concentrations (10(-9)-10(-8) M) caused inhibition of twitch responses of the rat vas deferens induced by nerve stimulation. These effects were competitively antagonized by yohimbine. Guanfacine and clonidine at relatively high concentrations (10(-6)-10(-4) M) produced contractions of the rat vas deferens which were antagonized by prazosin. These contractile responses were not much affected by denervation. Prazosin-sensitive contractions by guanfacine and clonidine were also observed in the rabbit aortic strip, which were not affected by reserpine pretreatment. In both tissues, the intrinsic activity of guanfacine was almost identical to that of norepinephrine, whereas that of clonidine was less than one half. Guanabenz and clonidine showed a competitive antagonistic effect against norepinephrine and phenylephrine in both the rat vas deferens and rabbit aorta, the antagonisms being similar in potency. The results indicate that all 3 drugs are potent agonists on the presynaptic alpha 2-adrenoceptor. In contrast, on the postsynaptic alpha 1-adrenoceptor, guanfacine and guanabenz showed only agonistic and antagonistic actions, respectively, whereas clonidine exhibited partial agonistic characteristics.

Adrenergic alpha-Agonists↗
PubMed1984

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

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.

Animals↗