Acetylcholine, Ca2+ overload and oscillatory potentials in isolated ventricular myocytes.
The events caused by overdrive-induced calcium overload were studied in guinea pig isolated ventricular myocytes. Overdrive may induce oscillatory potentials (Vos) and a prolonged depolarization (Vex), as well as the underlying currents (Ios and Iex, respectively). Acetylcholine (ACh) reduced or abolished these events, an action which was blocked by atropine. Norepinephrine exaggerated the effects of overdrive, and ACh markedly antagonized such an enhancement. Caffeine at low concentrations increased both Ios and Iex whereas at high concentrations caffeine abolished Ios but increased Iex. Quinacrine abolished both events. Voltage clamp depolarizing steps abolished Ios (and did not reverse it). Thus, the effects of Ca overload are antagonized by ACh in the absence and presence of sympathetic enhancement. Also, the mechanism underlying Ios appears to involve an electrogenic Ca extrusion and not an increase in a nonspecific conductance.
Yang
L
L
Department of Physiology, State University of New York, Brooklyn.
Vassalle
M
M
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D004594:Electrophysiology; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D011796:Quinacrine / Q000494:pharmacology
D002110:Caffeine; D011796:Quinacrine; D000109:Acetylcholine; D002118:Calcium; D009638:Norepinephrine