Vasopressin and angiotensin II in reflex regulation of heart rate: effect of water deprivation.
Vasopressin and angiotensin II in reflex regulation of heart rate: effect of water deprivation.
复制标题
加压素和血管紧张素 II 在心率反射调节中的作用：缺水的影响。
DOI：
10.1152/ajpregu.1992.263.4.r756
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Brooks,VL
中科院分区：
文献类型：
--
作者：
Brooks,VL
本研究验证了内源性血管紧张素II （ANG II）和抗利尿激素增强压力反射介导的无水犬心率增加和无水犬血浆ANG II和抗利尿激素浓度慢性升高的假设。通过检测心率对输注增加剂量的硝普赛（0.3、0.6、1.5和3.0微克。kg-1分钟-1）的反应来评估压力反射。测定了竞争性angii拮抗剂saralasin、V1-抗利尿素拮抗剂或V1/ v2 -抗利尿素联合拮抗剂单独或联合预处理犬对压力反射的影响。硝普塞输注导致心率呈剂量依赖性增加，与补水犬相比，缺水犬的心率反应更大，血浆中ANG II和血管加压素水平更高。单独的ANG II阻断抑制了缺水而非缺水犬的心率反射增加。在缺水和缺水的狗中，阻断v1 -抗利尿激素受体降低了对低血压的心率反应，但只有当ANG II受体也被阻断时才会产生这种效果。此外，给予萨拉拉西和V1/ v2 -血管加压素拮抗剂可进一步降低反射性心动过速。这些数据表明内源性抗利尿激素作用于V1和v2受体，可以放大低血压引起的心率增加。此外，这些结果进一步支持内源性ANG II的慢性升高在维持正常的气压反射功能中的生理作用。
This study tested the hypothesis that endogenous angiotensin II (ANG II) and vasopressin enhance baroreflex-mediated increases in heart rate in water-replete dogs and in dogs water deprived to chronically elevate plasma ANG II and vasopressin concentrations. The baroreflex was assessed by examining the heart rate response to infusion of increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 micrograms.kg-1.min-1). The effect on the baroreflex of pretreating the dogs with the competitive ANG II antagonist saralasin, a V1-vasopressin antagonist, or a combined V1/V2-vasopressin antagonist, alone or in combination, was determined. Nitroprusside infusion produced dose-dependent increases in heart rate, and the heart rate response was greater in water-deprived dogs in association with higher plasma levels of ANG II and vasopressin than in water-replete dogs. ANG II blockade alone depressed reflex increases in heart rate in water-deprived but not water-replete dogs. In both water-replete and water-deprived dogs, blockade of V1-vasopressin receptors reduced the heart rate response to hypotension, but this effect could be produced only when ANG II receptors were also blocked. In addition, administration of saralasin and the V1/V2-vasopressin antagonist led to a further reduction of the reflex tachycardia. These data suggest that endogenous vasopressin, acting at both V1- and V2-receptors, can amplify the increase in heart rate produced by hypotension. In addition, the results further support a physiological role for chronic elevations in endogenous ANG II in the maintenance of normal baroreflex function.