Circulatory effects of angiotensin II during anaesthesia, evaluated by real-time spectral analysis.

BACKGROUND: General anaesthesia may stimulate the renin-angiotensin system. Exogenous administration of angiotensin II elevates blood pressure mainly via increased total peripheral resistance caused by direct vasoconstrictor actions. It is also well established that the hypertensive effect of angiotensin II involves a cerebrally mediated component. The hypertensive effect of an intravascular infusion of angiotensin II is substantially reduced by isoflurane anaesthesia. A likely mechanism is that isoflurane anaesthesia reduces the cerebral component of the angiotensin II effect on blood pressure, which involves influences on autonomic nervous activity. In an experimental study in sheep we used real-time spectral analysis of arterial blood pressure signals to obtain information on parasympathetic, respectively, sympathetic autonomic nervous activity in response to angiotensin II administration during isoflurane anaesthesia.
METHODS: The study was performed on conscious and isoflurane-anaesthetized sheep that were subjected to an intracarotid infusion of angiotensin II (85 ng kg(-1) min(-1)) during 20 min followed by a recovery period of 30 min and thereafter an injection of the angiotensin II, AT1-receptor antagonist losartan (10 mg kg(-1)) i.v. Systemic and regional (renal and femoral) circulation was monitored in parallel to real-time spectral analysis of the arterial blood pressure signal.
RESULTS: Isoflurane anaesthesia reduced both magnitude and duration of the hypertensive response to angiotensin II infusion. The power spectral density in the frequency band that represents sympathetic activation, correlated to the changes in mean arterial pressure in conscious animals, but not during isoflurane anaesthesia.
CONCLUSION: We conclude that the cerebrally mediated component of the hypertensive effect of circulating angiotensin II is largely eliminated by isoflurane anaesthesia. Spectral power analysis of the blood pressure signal indicates that the cerebral angiotensin II effect involves activation of sympathetic nervous activity.