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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >V1a vasopressin receptors maintain normal blood pressure by regulating circulating blood volume and baroreflex sensitivity
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V1a vasopressin receptors maintain normal blood pressure by regulating circulating blood volume and baroreflex sensitivity

机译：V1a加压素受体通过调节循环血容量和压力反射敏感性来维持正常血压

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摘要

Arginine-vasopressin (AVP) is a hormone that is essential for both osmotic and cardiovascular homeostasis, and exerts important physiological regulation through three distinct receptors, V1a, V1b, and V2. Although AVP is used clinically as a potent vasoconstrictor (V1a receptor-mediated) in patients with circulatory shock, the physiological role of vasopressin V1a receptors in blood pressure (BP) homeostasis is ill-defined. In this study, we investigated the functional roles of the V1a receptor in cardiovascular homeostasis using gene targeting. The basal BP of conscious mutant mice lacking the V1a receptor gene (V1a(-/-)) was significantly (P < 0.001) lower compared to the wild-type mice (V1a(+/+)) without a notable change in heart rate. There was no significant alteration in cardiac functions as assessed by echocardiogram in the mutant mice. AVP-induced vasopressor responses were abolished in the mutant mice; rather, AVP caused a decrease in BP, which occurred in part through V2 receptor-mediated release of nitric oxide from the vascular endothelium. Arterial baroreceptor reflexes were markedly impaired in mutant mice, consistent with a loss of V1a receptors in the central area of baroreflex control. Notably, mutant mice showed a significant 9% reduction in circulating blood volume. Furthermore, mutant mice had normal plasma AVP levels and a normal AVP secretory response, but had significantly lower adrenocortical responsiveness to adrenocorticotropic hormone. Taken together, these results indicate that the V1a receptor plays an important role in normal resting arterial BP regulation mainly by its regulation of circulating blood volume and baroreflex sensitivity.
机译：精氨酸加压素（AVP）是一种对渗透和心血管体内稳态均必不可少的激素，并通过三个不同的受体V1a，V1b和V2发挥重要的生理调节作用。尽管在临床上将AVP用作循环休克患者的有效血管收缩剂（V1a受体介导的），但血管加压素V1a受体在血压（BP）稳态中的生理作用尚不清楚。在这项研究中，我们使用基因定位研究了V1a受体在心血管稳态中的功能。与野生型小鼠（V1a（+ / +））相比，缺乏V1a受体基因（V1a（-/-））的有意识突变小鼠的基础BP显着降低（P <0.001），而心率没有明显变化。经超声心动图评估，突变小鼠的心脏功能没有明显改变。在突变小鼠中，AVP诱导的血管加压反应消失了。相反，AVP导致BP下降，这部分是由于V2受体介导的一氧化氮从血管内皮的释放所致。在突变小鼠中，动脉压力感受器反射明显受损，这与压力反射控制中心区域的V1a受体丢失相一致。值得注意的是，突变小鼠的循环血量显着降低了9％。此外，突变小鼠的血浆AVP水平正常，分泌反应正常，但对促肾上腺皮质激素的肾上腺皮质反应显着降低。综上所述，这些结果表明，V1a受体主要通过调节循环血容量和压力反射敏感性而在正常的静息动脉BP调节中起重要作用。

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