2.6 ± 0.2 ml/g per min; P < 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 reninangiotensin system ( B P F 9 S ; l-Sar,8-Ala-angiotensin II; propranolol) but not by a-adrenergic blocking agents (phentolamine and ' phenoxybenzamine). Anesthesia blunted the renal vascular response to angiotensin II (P < 0.0005) whereas responsiveness to norepinephrine was increased (P < 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.A MAJOR cardiovascular response including reduced renal blood flow is often induced by anesthesia in man 1 " 1 and in experimental animals.5 " Although the mechanisms for these are poorly defined, anesthesia-induced activation of the renin-angiotensin system*' l 2 ' 1 4 is a possible cause, as the renal vasculature is especially sensitive to angiotensin I I i s . i6 H0Wever, there is considerable discrepancy between reports on the sensitivity of the renovascular bed to angiotensin.18 " 22 In man, for example, studies performed without anesthesia demonstrated a threshold response to angiotensin infused into the renal artery at doses generally below 10 ng/min," and the renal vessels were 100-fold more sensitive to angiotensin than to norepinephrine. In anesthetized animals, on the other hand, a number of studies have revealed a requirement for much higher doses of angiotensin 7 ' " " " and it has been suggested that the renal vessels are more sensitive to norepinephrine than to angiotensin." These discrepant results may be due to the fact that anesthesia can blunt renal vascular responses to angiotensin II,'-'" and perhaps reflect the frequent association of activation of the renin-angiotensin system and a reduction in vascular responsiveness to angiotensin I I . " It therefore seemed important to assess the role of renin-angi- Received May 27, 1975; accepted for publication October 13, 1975. otensin system activation in the renal vascular response to anesthesia. We have performed such a study in dogs with catheters chronically implanted in the renal artery. Using this model, we assessed the effects of barbiturate anesthesia and of sodium intake on renal perfusion and responsiveness to vasoconstrictor agents and appropriate blocking drugs. Methods SURGICAL PREPARATIONStudies were performed on 25 healthy, mongrel dogs, weighing 21-35 kg and selected for gentleness. In experiments in which surgery was performed, or when the effects of anesthesia per se were to be studied, anesthesia was induced with an initial intravenous dose of sodium pentobarbital (30 mg/kg) and maintained with periodic additional doses of 3-5 mg/kg of the same agent, to prevent spontaneous movement. At the time of preparative surgery a period of at least 60 minutes was allowed after the completion of procedures before vascular studies were performed; a 30-minute pe...

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