Medina P, Vila J M, Martinez M C, Aldasoro M, Chuan P, Lluch S
Departamento de Fisiología, Universidad de Valencia, Spain.
Eur J Clin Invest. 1996 Nov;26(11):966-72. doi: 10.1046/j.1365-2362.1996.2310543.x.
The effects of vasopressin were studied in isolated rings from branches (2-3 mm in external diameter) of human renal arteries obtained from 18 patients undergoing nephrectomy for non-obstructive neoplasia. In arterial rings under resting tension, vasopressin produced concentration-dependent and endothelium-independent contractions with an EC50 of 9.1 X 10(-10) molL-1. The vasopressin V1 receptor antagonist d(CH2)Tyr(Me)AVP (10(-6) molL-1) displaced the control curve to vasopressin 564-fold to the right in a parallel manner. In precontracted arterial rings and previously treated with the V1 antagonist (10(-6) molL-1) vasopressin caused endothelium-independent relaxation. The relaxation to vasopressin was reduced significantly by indomethacin (10(-6) molL-1) and unaffected by the V1/V2 receptor antagonist desGly d(CH2)5-D-Tyr(Et)ValAVP(10(-6) molL-1) or by NG-nitro-L-arginine methyl ester (10(-4) molL-1). These observations indicate that vasopressin is primarily a constrictor of human renal arteries by V1-receptor stimulation. Vasopressin causes prostaglandin-mediated dilation of human renal arteries only if V1-receptor blockade is present. The effects of vasopressin on human renal arteries may be relevant in those clinical situations characterized by increased plasma vasopressin levels.
对18例因非梗阻性肿瘤行肾切除术患者的人肾动脉分支（外径2 - 3毫米）的离体血管环进行了加压素作用的研究。在静息张力下的动脉环中，加压素产生浓度依赖性和内皮非依赖性收缩，EC50为9.1×10⁻¹⁰ mol/L。加压素V1受体拮抗剂d(CH₂)Tyr(Me)AVP（10⁻⁶ mol/L）使加压素的对照曲线平行右移564倍。在预先收缩且先前用V1拮抗剂（10⁻⁶ mol/L）处理过的动脉环中，加压素引起内皮非依赖性舒张。吲哚美辛（10⁻⁶ mol/L）显著降低了对加压素的舒张反应，而V1/V2受体拮抗剂desGly d(CH₂)₅ - D - Tyr(Et)ValAVP（10⁻⁶ mol/L）或NG - 硝基 - L - 精氨酸甲酯（10⁻⁴ mol/L）对此无影响。这些观察结果表明，加压素主要通过刺激V1受体使人类肾动脉收缩。仅当存在V1受体阻断时，加压素才会引起前列腺素介导的人类肾动脉舒张。加压素对人类肾动脉的作用可能与血浆加压素水平升高的临床情况有关。
