Suzuki S, Takeshita A, Imaizumi T, Hirooka Y, Yoshida M, Ando S, Nakamura M
Research Institute of Angiocardiology and Cardiovascular Clinic, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
J Clin Invest. 1989 Aug;84(2):427-34. doi: 10.1172/JCI114183.
Forearm vascular responses to arginine vasopressin (AVP) infused into a brachial artery in a wide range of infusion rates (0.05-2.0 ng/kg per min) were examined in 20 young healthy volunteers. Intraarterial AVP at lower doses (0.05 and 0.1 ng/kg per min) caused forearm vasoconstriction, whereas AVP at a dose of 0.2 ng/kg per min or higher caused forearm vasodilatation. The maximal forearm vasoconstriction was induced at the venous plasma AVP level of 76.3 +/- 8.8 pg/ml. Forearm vasodilatation was associated with the venous plasma AVP level of 369 +/- 43 pg/ml or higher. Forearm vasodilatation was the result of the direct effect of AVP since forearm blood flow and vascular resistance in the contralateral arm did not change. We attempted to explore the mechanisms involved in AVP-induced direct vasodilatation. The treatment with indomethacin, 75 mg/d for 3 d, did not alter AVP-induced forearm vasodilatation. In contrast, intraarterial infusion of isoosmolar CaCl2 totally prevented AVP-induced forearm vasodilatation. Intra-arterial CaCl2 also markedly attenuated forearm vasodilatation induced by intraarterial sodium nitroprusside, but did not alter forearm vasodilatation induced by intraarterial isoproterenol. These results indicate that the direct vascular effects of intra-arterial AVP on the forearm vessels are biphasic, causing vasoconstriction at lower doses and vasodilatation at higher doses. The direct vasodilatation induced by intraarterial AVP at higher doses is not mediated by prostaglandins but may involve cGMP-related mechanisms.
在20名年轻健康志愿者中，研究了前臂血管对以广泛输注速率（0.05 - 2.0 ng/kg每分钟）注入肱动脉的精氨酸加压素（AVP）的反应。较低剂量（0.05和0.1 ng/kg每分钟）的动脉内AVP引起前臂血管收缩，而剂量为0.2 ng/kg每分钟或更高的AVP引起前臂血管舒张。在前臂静脉血浆AVP水平为76.3±8.8 pg/ml时诱导出最大前臂血管收缩。前臂血管舒张与静脉血浆AVP水平369±43 pg/ml或更高有关。前臂血管舒张是AVP直接作用的结果，因为对侧手臂的前臂血流量和血管阻力没有变化。我们试图探究AVP诱导直接血管舒张所涉及的机制。吲哚美辛治疗，75 mg/d，持续3天，并未改变AVP诱导的前臂血管舒张。相反，动脉内输注等渗CaCl2完全阻止了AVP诱导的前臂血管舒张。动脉内CaCl2也显著减弱了动脉内硝普钠诱导的前臂血管舒张，但未改变动脉内异丙肾上腺素诱导的前臂血管舒张。这些结果表明，动脉内AVP对前臂血管的直接血管作用是双相的，较低剂量时引起血管收缩，较高剂量时引起血管舒张。较高剂量动脉内AVP诱导的直接血管舒张不是由前列腺素介导的，而是可能涉及与环磷酸鸟苷（cGMP）相关的机制。
