Medina P, Martínez M C, Aldasoro M, Vila J M, Chuan P, Lluch S
Departamento de Fisiología, Universidad de Valencia, Spain.
Eur J Pharmacol. 1996 Apr 11;300(3):221-5. doi: 10.1016/0014-2999(96)00006-4.
We studied the effects of vasopressin on isolated rings of human deferential artery and vas deferens (prostatic portion) obtained from patients undergoing radical cystectomy (n = 11) or prostatectomy (n = 10). Ring segments of artery or vas deferens were studied in organ bath experiments at optimal resting tension. In artery rings, vasopressin produced concentration-dependent, endothelium-independent contractions with an EC50 of 4.5 x 10(-10) M. The presence of NG-nitro-L-arginine methyl ester hydrochloride (10(-4) M), an inhibitor of nitric oxide synthase, did not change significantly (P > 0.05) the vasopressin-induced contraction. In ring preparations of the prostatic part of the vas deferens, vasopressin induced phasic contractions with an EC50 of 7.0 x 10(-9) M. The vasopressin V1 receptor antagonist, d(CH2)5Tyr(Me)AVP (10(-8) and 10(-6)), displaced to the right in parallel the control curve to vasopressin in artery and vas deferens rings. These results indicate that vasopressin exerts a powerful constrictor action on human deferential artery and vas deferens by direct stimulation of V1 receptors. It is concluded that the deferential artery may dampen the passage of blood to the vas deferens in circumstances characterized by increased plasma vasopressin levels.
我们研究了血管加压素对从接受根治性膀胱切除术的患者（n = 11）或前列腺切除术的患者（n = 10）获取的人输精管和输精管（前列腺部）离体环的影响。在器官浴实验中，于最佳静息张力下研究动脉或输精管的环段。在动脉环中，血管加压素产生浓度依赖性、不依赖内皮的收缩，其半数有效浓度（EC50）为4.5×10⁻¹⁰ M。一氧化氮合酶抑制剂盐酸NG-硝基-L-精氨酸甲酯（10⁻⁴ M）的存在并未显著改变（P>0.05）血管加压素诱导的收缩。在输精管前列腺部的环制备物中，血管加压素诱导相位性收缩，其EC50为7.0×10⁻⁹ M。血管加压素V1受体拮抗剂d(CH2)5Tyr(Me)AVP（10⁻⁸和10⁻⁶）使动脉和输精管环中血管加压素的对照曲线平行右移。这些结果表明，血管加压素通过直接刺激V1受体对人输精管和输精管发挥强大的收缩作用。得出的结论是，在血浆血管加压素水平升高的情况下，输精管动脉可能会抑制血液流向输精管。
