中枢血管紧张素Ⅱ在慢性应激大鼠颈动脉窦反射重调中的作用

Role of Central Angiotensin II in Carotid Sinus Baroreflex Resetting in Chronically Stressed Rat

目的 研究慢性应激大鼠颈动脉窦反射（ＣＳＲ）的功能变化，并观察中枢血管紧张素Ⅱ（ＡＮＧⅡ） 在其变化中的作用。方法 应激组大鼠随机足底电击２ 周。在麻醉下孤离颈动脉窦，用多道仪同步记录平均动脉压（ＭＡＰ）和窦内压（ＩＳＰ） 。应用五参数ｌｏｇｉｓｔｉｃ 函数拟合实验数据，并定量分析反射参数的变化。结果 慢性应激后ＣＳＲ 发生慢性重调，表现为调定点移向高ＩＳＰ区， 反射增益和ＭＡＰ反射范围减小；侧脑室（ＬＣＶ） 内注射ＡＮＧⅡ特异拮抗剂肌丙抗增压素后，与注射前相比，增益和ＭＡＰ反射范围增大，调定点减小，但仍高于非应激组。ＬＣＶ 注射ＡＮＧⅡ后非应激大鼠ＣＳＲ增益显著性下降，调定点增大；ＬＣＶ 内肌丙抗增压素预处理可完全阻断ＡＮＧⅡ的上述作用。结论 慢性应激时ＣＳＲ发生了重调，反射功能受到抑制，应激对ＣＳＲ

Objective The study was aims at investigating the effect of chronic stress on the performance of the carotid sinus reflex (CSR) and the modulation of central endogenous angiotensin II (ANGII). Methods The carotid sinus was isolated from the systemic circulation in anesthetized Wistar rats after two weeks of unpredictable footshock. The mean arterial pressure (MAP) and the intracarotid sinus pressure(ISP) were simultaneously recorded. The ISP-MAP relationship curve was fitted and constructed by a modified logistic function. Results In the stressed rats, injection of ANGII specific receptor antagonist saralasin into the lateral cerebral ventricle (LCV) produced a significant decrease in the set point and increases in both the reflex gain and the MAP range as compared with those before at before injection. But the set point was still significantly higher than that in the unstressed rats. In the unstressed rats, decreases in the reflex gain and the MAP range and increase in the set point were found after injection of ANG Ⅱ into LCV as compared with those before injection. The above actions of ANG Ⅱ injection were blocked by saralasin treatment. Conclusion Chronic stress may inhibit and reset the CSR function through central ANG Ⅱ.