Abstract

We had previously reported that drugs which stimulate beta-2 adrenergic receptors decreased the hyperkalemia produced by infused KCI and thus protected animals against KCI intoxication; these effects were mediated by an action of beta-2 agonists which enhanced tissue uptake of K+. In this study, cats were given an i.v. infusion of KCI which was not lethal in control animals. Acute adrenalectomy markedly increased the hyperkalemic and mortality responses to infused KCI. This impairment in K+ metabolism was corrected by the administration of epinephrine but not by hydrocortisone. Pretreatment with propranolol (which blocks beta-1 and beta-2 receptors) and H35/25 (which blocks beta-2 receptors) produced a similar impairment in K+ metabolism; on the other hand, practolol (which blocks beta-1 receptors) had little or no effect on the mortality and hyperkalemic responses to infused KCI. Evidence that KCI stimulates an adrenal release of catecholamines is presented. This stimulation of adrenal release may be important in conferring resistance to intoxication produced by infused KCI since the released amines can attenuate the KCI-induced hyperkalemia via a beta-2 action which enhances tissue uptake of K+.