Contributions of the sympathetic nervous system, vasopressin and baroreceptor function in brain angiotensin II excess-induced hypertension in the dog.

Abstract

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 of Ang II into the brain ventricle in conscious dogs, and then evaluated the hemodynamic responses to sole-innervated carotid artery occlusion(COR) after Ang II infusion and again after vagotomy in anesthetized dogs. Both acute(50ng/kg/min) and chronic(15ng/kg/min) infusion of Ang 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 CSF 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 Ang II treatment was restored by cutting the remaining vagus nerve. These results suggest that baroreceptor reflexes are impaired by the acute excess of Ang II in the brain, and it might be mediated through increased vagal afferent activity, changes in the central integration of low and high pressure baroreceptors, and a combination of both.