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

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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