The role of angiotensin in the canine renal vascular response to barbiturate anesthesia.

Abstract

The influence of barbiturate anesthesia on renal blood flow was assessed by the xenon washout method in trained dogs with catheters chronically implanted in the renal artery. Anesthesia induced with either thiopental sodium or pentobarbital sodium resulted in a striking reduction in renal blood flow (4.1 +/- 0.1 vs. 2.6 +/- 0.2 ml/g per min; P less than 0.001) without a change in arterial pressure. The reduction in blood flow was prevented by a high salt intake and partially reversed by agents which interrupt the renin-angiotensin system (BPF 9a; 1-Sar,8-Ala-angiotensin II; propranolol) but not by alpha-adrenergic blocking agents (phentolamine and phenoxybenzamine). Anesthesia blunted the renal vascular response to angiotensin II (P less than 0.0005) whereas responsiveness to norepinephrine was increased (P less than 0.05). We conclude that barbiturate anesthesia induces a major, angiotensin-mediated renal vascular response which must be considered in the interpretation of experiments performed under these conditions.