Norepinephrine-induced reflex bradycardia after central administration of angiotensin II

Central angiotensin effects may include baroreceptor alterations and/or ventilated, were given angiotensin intravertebrally (10 ng/kg/min), into a lateral cerebroventricle (0.4 microgram/min) or intravenously (10 ng/kg/min). Surgery was completed under methoxyflurane anesthesia; wounds were periodically infiltrated with viscous tetracaine and the methoxyflurane discontinued. The experiments were performed with the brain unanesthetized to optimize detection of an angiotensin effect on the cardioinhibitory component of the baroreceptor reflex. Bradycardia was evoked by norepinephrine injections (2 microgram/kg i.v.). Intraventricular and intravertebral angiotensin increased basal mean blood pressure 16 mm Hg (p less than 0.05); norepinephrine-induced pressor responses and bradycardia were unaffected by the peptide. Intravenous angiotensin did not affect basal blood pressure; a 16 mm Hg increase (p less than 0.05) in the norepinephrine pressor response with no change in bradycardia was observed. Atropine reversed the norepinephrine bradycardia and increased the pressor response in all cats, thus demonstrating the integrity of the reflex. We conclude that centrally administered angiotensin produces no change in the cardioinhibitory reflex to an acute pressor stimulus. The possibility of a peripheral effect of the peptide exists. The hypertensive response observed in the conscious spinal cats after central angiotensin infusions could be due to vasopressin release and/or action of the peptide at cardiovascular sites at high spinal levels.