Abstract

In rats we assessed the role of the sympathetic nervous system in the increase of plasma renin activity (PRA) following induction of anesthesia by urethane, ether, or pentobarbital and the role of these increased levels of PRA in the maintenance of blood pressure.Urethane and ether induced marked, sustained increases in PRA. Pentobarbital was less effective in this regard. Propranolol inhibited the response of PRA to urethane and ether in a dose-dependent manner but not the renin response to pentobarbital. Similarly, neonatal sympathectomy with 6-hydroxydopamine together with removal of the adrenal medulla prevented the renin response to urethane but not to pentobarbital.Blood pressure changed only slightly during urethane anesthesia, showed a sustained decrease during ether anesthesia, and a gradual return to normal following a marked initial drop during pentobarbital anesthesia. Saralasin pretreatment induced a marked decrease (40–45 mmHg; 1 mmHg = 133.322 Pa) in blood pressure during urethane anesthesia and smaller (10–20 mmHg) additional decreases during ether and pentobarbital anesthesia. In contrast, propranolol pretreatment did not significantly affect blood pressure during ether anesthesia and affected it to a minor degree (by 10–15 mmHg) during urethane and pentobarbital anesthesia.The results indicate that the increases in PRA following induction of anesthesia by urethane or ether, but not by pentobarbital, are mediated through the peripheral sympathetic nervous system via β adrenoceptors. The rennin–angiotensin system appears to be essential for the maintenance of a normal blood pressure during urethane anesthesia but plays a less prominent role in this regard during ether and pentobarbital anesthesia. The propranolol studies suggest that the hypotensive effect of propranolol through blockade of the renin response during urethane- and ether-induced anesthesia is masked by a pressor effect of propranolol.

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