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由血管紧张素和氯化钠引发的不同交感神经反应。

Differential sympathetic responses initiated by angiotensin and sodium chloride.

作者信息

Tobey J C, Fry H K, Mizejewski C S, Fink G D, Weaver L C

出版信息

Am J Physiol. 1983 Jul;245(1):R60-8. doi: 10.1152/ajpregu.1983.245.1.R60.

DOI:10.1152/ajpregu.1983.245.1.R60
PMID:6869578
Abstract

Angiotensin II (ANG II) and NaCl act on central receptors to cause pressor responses that may be mediated in part by the sympathetic nervous system. The inhibitory or excitatory nature of effects on central sympathetic outflow are not well defined. This study was undertaken to evaluate further the potential contribution of the sympathetic nervous system to central actions of angiotensin or hypertonic NaCl. Experiments were performed using anesthetized, sinoaortic denervated, vagotomized cats. Intracarotid injection of NaCl produced increased splenic sympathetic nerve activity and decreased renal sympathetic nerve activity. Intracerebroventricular (icv) administration of NaCl caused slight excitatory responses in splenic nerves and no change in renal nerve activity. Intracarotid injection of ANG II caused significantly greater splenic than renal excitation. Administration of ANG II icv caused excitation of splenic nerve activity and no change in renal nerve activity. These findings illustrate that stimulation of sodium-sensitive and angiotensin-sensitive CNS receptors produces differential responses in sympathetic outflow. These differential sympathetic responses may contribute to the complex cardiovascular responses to increased plasma or brain concentrations of angiotensin or sodium.

摘要

血管紧张素II(ANG II)和氯化钠作用于中枢受体,引起升压反应,这可能部分由交感神经系统介导。对中枢交感神经流出的抑制或兴奋作用的性质尚未明确界定。进行这项研究是为了进一步评估交感神经系统对血管紧张素或高渗氯化钠中枢作用的潜在贡献。实验使用麻醉、去窦主动脉神经和迷走神经切断的猫进行。颈动脉内注射氯化钠可使脾交感神经活动增加,肾交感神经活动减少。脑室内(icv)注射氯化钠可使脾神经产生轻微兴奋反应,而肾神经活动无变化。颈动脉内注射ANG II引起的脾兴奋明显大于肾兴奋。icv注射ANG II可使脾神经活动兴奋,而肾神经活动无变化。这些发现表明,刺激钠敏感和血管紧张素敏感的中枢神经系统受体会在交感神经流出中产生不同的反应。这些不同的交感神经反应可能有助于解释对血浆或脑内血管紧张素或钠浓度升高所产生的复杂心血管反应。

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