Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.
Vasopressin-mediated forearm vasodilation in normal humans. Evidence for a vascular vasopressin V2 receptor.
复制标题
正常人加压素介导的前臂血管舒张。
DOI：
10.1172/jci114182
复制
发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Creager,MA
中科院分区：
文献类型：
--
作者：
Hirsch,AT;Dzau,VJ;Majzoub,JA;Creager,MA
精氨酸加压素 (AVP) 是一种有效的血管加压剂和抗利尿神经激素。然而，当静脉注射给人类时，AVP 会引起前臂血管舒张。这种效应归因于交感神经退缩，继发于 AVP 诱导的压力感受器敏化。 AVP 也直接引起前臂血管舒张的可能性尚未得到检验。因此，通过研究前臂血流（FBF）对动脉内（IA）AVP输注（0.01-1.0 ng/kg/min）的反应来确定AVP的直接作用。 IA AVP 的输注以剂量依赖的方式增加了输注臂的 FBF (96%)，但不增加对照组。在用 V1 拮抗剂 (AVP-A) 预处理之前和之后确定了特定 AVP V1 受体在介导 FBF 反应中的作用。单独使用 AVP-A 对 FBF 没有影响，但 AVP 和 AVP-A 共同给药可增强血管舒张反应 (223%)。 IA 输注 V2 激动剂 1-脱氨基[8-D-精氨酸]加压素可引起 FBF 剂量依赖性增加。这些发现表明，AVP 在人类前臂引起直接的、剂量依赖性的血管舒张，这可能是由 V2 血管加压素受体介导的。相比之下，AVP 输注引起指端血管收缩，但被 AVP-A 阻断，而 dDAVP 不影响指端血流。因此，AVP 诱导区域选择性血管效应，同时发生前臂血管舒张和手指血管收缩。
Arginine vasopressin (AVP) is a potent vasopressor and antidiuretic neurohormone. However, when administered intravenously to humans, AVP causes forearm vasodilation. This effect has been attributed to sympathetic withdrawal, secondary to AVP-induced sensitization of baroreceptors. The possibility that AVP also causes forearm vasodilation directly has not been examined. Accordingly, the direct effect of AVP was determined by studying the forearm blood flow (FBF) response to intraarterial (IA) AVP infusion (0.01-1.0 ng/kg per min). Infusion of IA AVP increased FBF (96%) in the infused arm, but not the control arm, in a dose-dependent manner. The role of specific AVP V1 receptors in mediating this FBF response was determined before and after pretreatment with a V1 antagonist (AVP-A). AVP-A alone had no effect on FBF, but coadministration of AVP and AVP-A potentiated the vasodilatory response (223%). IA infusion of the V2 agonist, 1-desamino[8-D-arginine] vasopressin, caused a dose-dependent increase in FBF. These findings suggest that AVP causes direct, dose-dependent vasodilation in the human forearm that may be mediated by V2 vasopressinergic receptors. In contrast, AVP infusion caused digital vasoconstriction that was blocked by AVP-A, whereas dDAVP did not affect digital blood flow. Thus, AVP induces regionally selective vascular effects, with concurrent forearm vasodilation and digital vasoconstriction.