Renin release by pentobarbital anesthesia in the rat: A role for vascular mechanisms

Studies were undertaken in intact rats to characterize the renin response to pentobarbital anesthesia and the mechanisms involved in this response. Aortic and peritoneal cavity cannulas were previously implanted to allow drug infusion, blood sampling and anesthesia to be performed without stress. A sustained 2–3- fold increase in plasma renin concentration (PRC) and a 10–15 mm Hg depression of mean arterial pressure were found in pentobarbital anesthesia. Circulating levels of epinephrine and norepinephrine were unchanged. Sympathetic stimulation by tyramine did not decrease and chronic renal denervation did not abolish the PRC rise by pentobarbital. Phenoxybenzamine given to conscious or anesthetized animals elevated PRC to similar levels. Propranolol was effective in suppressing PRC in anesthetized animals, regardless of the presence or absence of phenoxybenzamine. We concluded that the renin response to pentobarbital anesthesia is unrelated to changes in sympatho-adrenal activity. The response appears to be mediated by beta-adrenergic receptors. It is postulated that pentobarbital- induced relaxation of afferent arterioles or JG cells exposes previously concealed beta-receptor sites which increase the signal for the release of renin.