Renin release, an artifact of anesthesia and its implications in rats

Abstract

In our attempt to find an anesthetic agent which did not influence the renin-angiotensin system in the rat, the effect of widely used injectable and gaseous anesthetics and narcotic agents on renin release was chacterized. All of the agents studied induced dose- and time-related increases in serum renin activity when administered in anesthetic doses. Preliminary experiments in anesthetic doses. Preliminary experiments indicated that cardiovascular effects were highly variable, giving little insight into the relationship between renin release and cardiovascular changes. Propranolol impaired most of the anesthesia-induced renin release and impaired aldosterone release with the one agent (urethane) studied. Renin release by two anesthetic agents (ketamine and urethane) appeared to be mediated premarily through the beta-adrenermediated primarily through the beta-adrenergic receptor mechanism, but equivocal results were obtained with other agents (pentobarbital and morphine). It is possible that other anesthetics, as with urethane, may induce aldosterone release by way of renin release. This anesthesia-induced renin release and the extensive biologic activities of angiotensin and aldosterone suggest a potential for influencing many investigations, particularly those involving cardiovascular and endocrine systems.