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

脑血管紧张素II在血压控制中枢机制中的作用及其对高血压的意义。

• 批准号: 63570410
• 负责人: UENO Yuji
• 金额: $ 1.28万
• 依托单位: Wakayama Medical College
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1988
• 资助国家: 日本
• 起止时间: 1988 至 无数据
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-63570410/
• 关键词: Central mechanisms of blood pressure control; Hypertension; Angiotensin II; Vasopressin; Baroreceptor reflex; Cardiopulmonary baroreceptor; 迷走神経

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

为探讨脑血管紧张素Ⅱ（ANG Ⅱ）对交感神经系统、加压素（AVP）及高、低压压力感受器系统的主要作用，我们观察了清醒犬脑室灌注ANG Ⅱ急性（1小时）和慢性（1周）引起的血流动力学和神经体液特性。然后在麻醉犬中评估血管紧张素II（Ang II）灌注和迷走神经切断后对单侧神经支配的颈动脉闭塞（COR）的血流动力学反应。此外，采用迷走神经冷阻滞技术，观察脑室灌注血管紧张素Ⅱ（Ang Ⅱ）和精氨酸加压素（AVP）对心肺压力感受性反射的影响。急性（50 ng/kg/min）和慢性（15 ng/kg/min）输注And II均引起动脉压显著升高，而心率无变化。急性或慢性Ang II治疗均未引起血浆和脑脊液（CSF）中血浆肾素活性和去甲肾上腺素的显著变化，而血浆和脑脊液（CSF） ...更多信息 急性Ang Ⅱ治疗组血浆F水平升高，慢性Ang Ⅱ治疗组血浆F水平无明显变化。与慢性Ang II或假手术治疗相比，急性Ang II治疗的COR变钝。在急性血管紧张素II治疗中，通过切断剩余的迷走神经恢复了对颈动脉闭塞的钝性升压反应。在麻醉和窦主动脉去神经犬中，VCB可显著增加平均动脉压、心输出量和血管阻力。脑室注射Ang Ⅱ（50- 200 ng/kg）可明显降低心输出量和血管阻力，从而减弱VCB的上述血流动力学反应。然而，当将AVP（4-10 g/kg）应用于CSF时，未观察到对VCB的血流动力学反应的实质性变化。这些结果表明，动脉和心肺压力感受器反射受损的急性过量的血管紧张素II在大脑中，它可能是通过在低压和高压压力感受器的中央整合的变化介导的。少

项目成果

Yuji Ueno; et al.: "Characteristics of hormonal and neurogenic mechanisms of DOC-induced hypertension." Hypertension. 11. 172-177 (1988)

上野雄二;

Yuji Ueno;et al.: Hypertension. 11. I-172-I-177 (1988)

Yuji Ueno；等人：高血压。

Masato Kuchii; et al.: Annual Review Cardiology; Hypertension and catecholamine.Chugai Igaku Co. LTD., 388 (1988)

口井正人；

Yuji Ueno,et al.: Hypertension. 11. I-172-I-177 (1988)

Yuji Ueno 等：高血压。

口井正人 他: "Annual Review循環器;高血圧とカテコールアミン" 中外医学社, 388 (1988)

Masato Kuchii 等人：“心血管系统年度回顾；高血压和儿茶酚胺”Chugai Igakusha，388 (1988)