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中枢血管紧张素II受体参与慢性应激大鼠的颈动脉窦反射重调定。

Central ANG II receptor involved in carotid sinus reflex resetting in chronically stressed rats.

作者信息

Qian Z M, Xiao D S, Huang W Q, Tang P L, Xu B

机构信息

Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon.

出版信息

Physiol Behav. 1997 Aug;62(2):241-7. doi: 10.1016/s0031-9384(97)00109-1.

Abstract

The performance of carotid sinus baroreceptor reflex (CSR) was characterized in chronically stressed rats by changing intracarotid sinus pressure (ISP) and constructing ISP-MAP (mean arterial pressure) relationship curve. The role of central angiotensin II (ANG II) receptors in the changes of CSR performance induced by chronic stress was determined. Rats were subjected to foot-shock stress for two weeks. The carotid sinus was isolated from the systemic circulation and the ISP changed in a stepwise manner. The results showed that in chronically stressed rats, ISP-MAP relationship curve shifted upward, the set point was significantly higher than that obtained from the unstressed group, and the reflex gain and the MAP range were significantly smaller than those in unstressed rats. After intracerebroventricular injection of saralasin (20 ng), MAP range was augmented and the set point decreased significantly. Injection of vehicle did not lead any significant differences between the parameters of the reflex measured before or after injection in either the stressed or the unstressed rats. Furthermore, administration of ANG II (10 microg) induced a significant increase in the set point and decrease in the reflex gain in the unstressed rats. The responses of CSR to ANG II were completely blocked by pretreatment of saralasin. These findings suggest that chronic stress could induce the decreased CSR function in the normotensives and central ANG II receptors involved in the resetting of CSR in the chronically stressed rats.

摘要

通过改变颈内动脉窦压力(ISP)并构建ISP-平均动脉压(MAP)关系曲线,来表征慢性应激大鼠的颈动脉窦压力感受器反射(CSR)性能。确定了中枢血管紧张素II(ANG II)受体在慢性应激诱导的CSR性能变化中的作用。大鼠接受两周的足部电击应激。将颈动脉窦与体循环隔离,ISP以逐步方式改变。结果表明,在慢性应激大鼠中,ISP-MAP关系曲线向上移位,设定点明显高于未应激组,反射增益和MAP范围明显小于未应激大鼠。脑室内注射沙拉新(20 ng)后,MAP范围增大,设定点明显降低。注射溶剂在应激或未应激大鼠中均未导致注射前后测量的反射参数出现任何显著差异。此外,给予ANG II(10μg)可使未应激大鼠的设定点显著增加,反射增益降低。沙拉新预处理可完全阻断CSR对ANG II的反应。这些发现表明,慢性应激可导致正常血压者CSR功能下降,且中枢ANG II受体参与慢性应激大鼠CSR的重调定。

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