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Cardiovascular Research Laboratories, Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7
Control of contraction and relaxation by membrane
potential was investigated in voltage-clamped guinea pig ventricular
myocytes at 37°C. Depolarization initiated phasic contractions,
followed by sustained contractions that relaxed with repolarization.
Corresponding Ca2+ transients were observed with fura 2. Sustained responses were ryanodine sensitive and exhibited sigmoidal
activation and deactivation relations, with half-maximal voltages near
46 mV, which is characteristic of the voltage-sensitive release
mechanism (VSRM) for sarcoplasmic reticulum Ca2+.
Inactivation was not detected. Sustained responses were insensitive to
inactivation or block of L-type Ca2+ current
(ICa-L). The voltage dependence of sustained
responses was not affected by changes in intracellular or extracellular Na+ concentration. Furthermore, sustained responses were
not inhibited by 2 mM Ni2+. Thus it is improbable that
ICa-L or Na+/Ca2+ exchange
generated these sustained responses. However, rapid application of 200 µM tetracaine, which blocks the VSRM, strongly inhibited sustained
contractions. Our study indicates that the VSRM includes both a phasic
inactivating and a sustained noninactivating component. The sustained
component contributes both to initiation and relaxation of contraction.
voltage-sensitive release mechanism; calcium-induced calcium release; excitation-contraction coupling; calcium transients
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