Influence of forebrain lesions and isoflurane anaesthesia, respectively, on responses to the intracarotid infusion of angiotensin II in sheep.

In conscious sheep, lesions involving the anterior wall of the third cerebral ventricle extinguished the dipsogenic and cortisol releasing effects of 10 min intracarotid (i.c.) infusions of angiotensin II (Ang II) (20 pmol kg-1 min-1). The sustained hypertension obtained in response to i.c. Ang II in the intact animal was not significantly changed by the forebrain lesions. Pronounced, but short-lasting tachycardia immediately developed in response to i.c. Ang II in control animals. After a 1 min return to initial values the heart rate (HR) rose to about 20 beats min-1 above pre-infusion level during the remaining infusion period. After a brief post-infusion fall, HR retook that level. It then gradually declined but did not return to initial level until about 25 min later. During isoflurane anaesthesia in the latter animals carotid blood pressure (cBP) was reduced by approximately 30% while the HR was more than doubled. The cBP rise in response to i.c. Ang II infusion was < 50% of that seen in awake animals and the pressure returned to initial level within approximately 5 min after the end of the infusion. The infusion did not influence the HR. This study provides support for the idea that blood borne Ang II, bound at cerebral sites posterior to the hypothalamic region, continues to have cardiovascular effects for approximately 20 min after the concentration in the blood has returned to pre-infusion level.