beta(2)-adrenoceptors and ventricular fibrillation

beta -Adrenoceptor antagonists significantly reduce the incidence of sudden cardiac death in patients with contractile dysfunction. Contractile dysfun ction is associated with a decline in beta (1)-adrenoceptors, no change in the number of beta (2)-adrenoceptors, and an increased responsiveness to be ta (2)-adrenoceptor stimulation. Selective beta (2)-adrenoceptor blockade p revents ventricular fibrillation in a canine model of sudden cardiac death. Cardiac beta (2)-adrenoceptor stimulation increases L-type Ca2+ currents, but unlike beta (1)-adrenoceptor stimulation, it fails to elicit phospholam ban phosphorylation, Restoration of resting diastolic [Ca2+] following beta (2)-adrenoceptor-mediated increases in Ca2+ influx is more dependent on Na +/Ca2+ exchange, which generates an arrhythmogenic transient inward current that can trigger ventricular fibrillation. (C) 2000 Elsevier Science Inc. All rights reserved.