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.
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