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血管紧张素II对大鼠延髓头端腹外侧区压力感受性神经元的抑制作用。

Inhibitory effects of angiotensin II on barosensitive rostral ventrolateral medulla neurons of the rat.

作者信息

Bertram D, Coote J H

机构信息

CNRS UMR 5014, Faculté de Pharmacie, Lyon, France.

出版信息

Clin Exp Pharmacol Physiol. 2001 Dec;28(12):1112-4. doi: 10.1046/j.1440-1681.2001.03583.x.

Abstract
  1. The brain renin-angiotensin system can influence arterial baroreceptor reflex control of blood pressure (BP) through both direct and indirect effects on sympathetic premotor neurons of the rostral ventrolateral medulla (RVLM). The present study examined the direct effect of angiotensin (Ang) II applied by microiontophoresis on the ongoing activity of single RVLM neurons. 2. In 26 urethane-anaesthetized Wistar rats, recordings of single unit activities of barosensitive RVLM neurons were made from one barrel of a six-barrel micropipette assembly. The other five barrels were filled with either L-glutamate, AngII, valsartan (an AT1 receptor antagonist), PD 123177 (an AT2 receptor antagonist) and saline. All drugs were applied by microiontophoresis. 3. Mean BP was 83 +/- 3 mmHg. Application of AngII inhibited the ongoing activity of RVLM neurons, identified as barosensitive because their activity was inhibited by a phenylephrine- induced increase in BP, from 12.6 +/- 1.5 to 5.4 +/- 1.1 Hz (n=24; P < 0.001). Angiotensin II also inhibited the glutamate-evoked excitation of barosensitive RVLM neurons from 15 +/- 3 to 5.8 +/- 2.0 Hz (n=6; P < 0.001). Valsartan significantly increased neuronal activity from 9.5 +/- 2.3 to 13.5 +/- 3.2 Hz (n=7, P < 0.01), whereas PD 123177 significantly decreased neuronal activity from 13.5 +/- 3.5 to 9.9 +/- 2.8 Hz (n=13; P < 0.01). 4. The results suggest that AngII exerts a tonic inhibitory effect on barosensitive RVLM neurons, which is presumably mediated through AT1 receptor stimulation.
摘要
  1. 脑肾素-血管紧张素系统可通过对延髓头端腹外侧区(RVLM)交感运动前神经元的直接和间接作用,影响动脉压力感受器对血压(BP)的反射控制。本研究通过微离子电泳施加血管紧张素(Ang)II,检测其对单个RVLM神经元自发放电活动的直接影响。2. 对26只乌拉坦麻醉的Wistar大鼠,用六管微电极组件的一个管记录压力敏感RVLM神经元的单位活动。其他五个管分别填充L-谷氨酸、AngII、缬沙坦(一种AT1受体拮抗剂)、PD 123,177(一种AT2受体拮抗剂)和生理盐水。所有药物均通过微离子电泳施加。3. 平均血压为83±3 mmHg。施加AngII可抑制RVLM神经元的自发放电活动,这些神经元被确定为压力敏感型,因为它们的活动会被去氧肾上腺素诱导的血压升高所抑制,自发放电频率从12.6±1.5 Hz降至5.4±1.1 Hz(n = 24;P < 0.001)。血管紧张素II还可抑制压力敏感RVLM神经元由谷氨酸诱发的兴奋,频率从15±3 Hz降至5.8±2.0 Hz(n = 6;P < 0.001)。缬沙坦可使神经元活动显著增加,从9.5±2.3 Hz增至13.5±3.2 Hz(n = 7,P < 0.01),而PD 123,177可使神经元活动显著降低,从13.5±3.5 Hz降至9.9±2.8 Hz(n = 13;P < 0.01)。4. 结果表明,AngII对压力敏感RVLM神经元具有持续性抑制作用,这可能是通过刺激AT1受体介导的。

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