The authors tested in dogs the hypothesis that beta-adrenoceptor blockade might alter the time course or magnitude of serum potassium (K+) changes following the administration of succinylcholine (SCh). The results indicate that the normal increase in K+ induced by SCh (1 mg/kg intravenously) is exaggerated in the presence of propranolol-induced (0.25 mg/kg), beta-adrenoceptor blockade. Specifically, a peak increase of 1.7 mEq/1 (43%) over control K+ was noted in the beta-blocked dogsversusa 0.5 mEq/l (13%) increase in control dogs. The peak increase in K+ occurred later in the beta-blocked dogs (60–90 min post-SCh)versuscontrol dogs (30 min post-SCh). The authors postulate that these results reflect impairment of intracellular uptake of the SCh-induced acute K+ load secondary to beta-adrenoceptor blockade. Additionally, in a third group of dogs, diazepam in a dose of 0.5 mg/kg attenuated the K+ increases (1 mEq/1—24%) following SCh in beta-blocked dogs. Whether these data can be extrapolated to beta-adrenoceptor blocked patients remains a matter for further investigation. In the interim, periodic monitoring of K+ is warranted in any patient receiving medications known to alter the state of activity of the beta-adrenoceptor. In particular, careful consideration must be given to the potential impact of various interventions (SCh administration, K+ infusion) on K+ levels in beta-adrenoceptor blocked patients.