Role of brain angiotensin II in the central mechanism of blood pressure control and its significance for hypertension.

为确定脑血管紧张素II(Ang II)对交感神经系统、加压素(AVP)和高低压压力感受器系统的主要作用，我们观察了急性(1小时)和慢性(1周)脑室注射Ang II或Ang II对清醒犬的血流动力学和神经体液特性的影响，并评价了Ang II注射后和迷走神经切断后再次支配颈动脉闭塞(COR)的血流动力学反应。采用迷走神经冷阻滞法观察脑室注射血管紧张素Ⅱ和血管紧张素转换酶对心肺压力感受器反射的影响。急性(50 ng/kg/min)和慢性(15 ng/kg/min)注射And II均导致动脉压显著升高，而心率没有变化。急性和慢性血管紧张素Ⅱ治疗对血浆肾素活性、血浆和脑脊液去甲肾上腺素均无明显影响，而血浆和CS…AVP的F水平在急性Ang II组升高更多，而在慢性Ang II组则无明显变化。与慢性血管紧张素Ⅱ或假手术组相比，急性血管紧张素Ⅱ治疗组的COR变钝。在急性血管紧张素Ⅱ治疗中，切断剩余的迷走神经可以恢复颈动脉闭塞后迟钝的升压反应。VCB能显著增加麻醉犬和失主动脉神经犬的平均动脉压、心输出量和血管阻力。脑室注射血管紧张素转换酶II(50-200 ng/kg)可显著降低心输出量和血管阻力，从而减弱VCB引起的上述血流动力学反应。然而，脑脊液中加入AVP(4-10g/kg)后，对VCB的血流动力学反应无明显改变。这些结果表明，动脉和心肺压力感受器反射都受到脑内血管紧张素Ⅱ的急性过量的损害，这可能是通过改变低压和高压压力感受器的中枢整合来实现的。较少

To determine the principal effects of brain angiotensin (ANG)II on the sympathetic nervous system, vasopressin (AVP), and the high and low pressure baroreceptor systems, we observed the hemodynamic and neurohumoral characteristics induced by the acute (1-hr) and chronic (1-wk) infusion or Ang II into the brain ventricle in conscious dogs, and then evaluated the hemodynamic responses to soleinnervated carotid artery occlusion (COR) after Ang II infusion and again after vagotomy in anesthetized dogs. In addition, the effects of Ang II and AVP infused into the brain ventricle on the cardiopulmonary baroreceptor reflex were examined using vagal cold block techniques. Both acute (50ng/kg/min) and chronic (15ng/kg/min) infusion of And II caused a significant rise in arterial pressure without changes in heart rate. Neither acute nor chronic Ang II treatment produced significant changes in plasma renin activity and norepinephrine in plasma and cerebrospinal fluid (CSF), while the plasma and CS … More F level of AVP was increased in the acute Ang II treatment, but not in the chronic Ang II treatment. The COR was blunted in the acute Ang II treatment compared with those obtained in the chronic Ang II or sham treatment. The blunted pressor response to carotid occlusion in the acute AngII treatment was restored by cutting the remaining vagus nerve. A significant increase in mean arterial pressure, cardiac output and vascular resistance was produced by VCB in anesthetized and sino-aortic denervated dogs. These hemodynamic responses to VCB were attenuated by Ang II (50-200ng/kg) treatment into the brain ventricle, resulting from the marked decrease in cardiac output and vascular resistance. However, a substantial change in hemodynamic responses to VCB was not observed when AVP (4-10 g/kg) was applied into CSF. These results suggest that both arterial and cardiopulmonary baroreceptor reflexes are impaired by the acute excess of Ang II in the brain, and it might be mediated through changes in the central integration of low and high pressure baroreceptors. Less