Activation of the central vasopressin system: a common pathway for several centrally acting pressor agents.
Activation of the central vasopressin system: a common pathway for several centrally acting pressor agents.
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中枢加压素系统的激活：几种中枢作用升压药的共同途径。
DOI：
10.1152/ajpregu.1986.251.3.r476
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Eskridge,SL
中科院分区：
文献类型：
--
作者：
Gruber,KA;Eskridge,SL
高渗盐水（HS）和血管紧张素II（ANG II）通过中枢或外周给药产生前脑介导的中枢神经系统（CNS）依赖性升压作用。虽然这些效应中的大多数是由于增加的中枢交感神经驱动和心脏压力感受器反射的抑制，来自血管加压素（Vp）受体拮抗剂的外周输注的证据表明，部分血压升高可能是由于循环Vp。我们现在报告，通过第四脑室输注Vp受体拮抗剂，阻断大鼠中枢神经系统Vp受体，减弱了侧脑室输注HS，ANG II或高渗葡萄糖（HG）的升压反应的70%以上。静脉注射Vp拮抗剂只能阻断40%的HS反应。在遗传性Vp缺乏的大鼠（尿崩症大鼠）侧脑室输注HS时，未获得升压反应。由于集中管理VP自主神经系统的影响，是类似的HS或ANG II引起的，我们的研究结果表明，中枢神经系统VP可能提供前脑作用升压剂和自主神经系统调节之间的联系。最后，HG产生的升压效应与HS具有相同的峰值反应。然而，与HS反应不同，在10分钟输注期间，HG的升压效应在约5分钟内恢复到基线。因此，在钠受体与β受体激活所产生的升压反应中似乎存在定量差异。
Hypertonic saline (HS) and angiotensin II (ANG II) administered centrally or peripherally produce a forebrain-mediated central nervous system-(CNS) dependent pressor action. Although the majority of these effects are due to increased central sympathetic drive and inhibition of the cardiac baroreceptor reflex, evidence from peripheral infusions of vasopressin (Vp) receptor antagonists have suggested that part of the blood pressure increase may be due to circulating Vp. We now report that blockade of CNS Vp receptors in rats, via a fourth ventricle infusion of a Vp receptor antagonist, attenuated greater than 70% of the pressor response to lateral ventricle infusion of HS, ANG II, or hypertonic glucose (HG). Intravenous administration of the Vp antagonist could block only 40% of the HS response. When lateral ventricle infusion of HS was performed in rats with a hereditary lack of Vp (diabetes insipidic rats) no pressor response was obtained. Because centrally administered Vp has autonomic nervous system effects that are similar to those induced by HS or ANG II, our results suggest that CNS Vp may provide a link between forebrain acting pressor agents and autonomic nervous system regulation. Finally, HG produced a pressor effect that had an equivalent peak response to HS. However, unlike the HS response, the pressor effect to HG returned to base line within approximately 5 min during a 10-min infusion. Thus there appears to be a quantitative difference in the pressor responses produced by activation of sodium vs. osmoreceptors.