Ventricular automaticity induced by bromobenzoyl-methyladamantylamine (BMA) in different membrane potential ranges in guinea pig heart.
The electrophysiological effects of bromobenzoyl - methyladamantylamine ( BMA ) were investigated in isolated electrically driven right ventricular papillary muscles of guinea pigs using conventional glass-microelectrode technique. BMA markedly increased the action potential duration, depolarized the membrane, reduced the maximum rate of depolarization (Vmax) and induced pacemaker-like action potentials. In ventricular myocardium depolarized partially (up to --40 mV) by incubation with 26 mM K+-Krebs solution, BMA induced slow action potentials. In these preparations, BMA was also able to evoke automaticity. Since the pacemaker activity occurring in the voltage range of --90 mV to --60 mV has been attributed to the deactivation of a pacemaker K+ current labelled IK2, and that occurring in the plateau range (from --40 mV to +10 mV) has been attributed to the deactivation of an outward plateau K+ current labelled IX1 , it can be concluded that BMA may inhibit both IK2 and IX1 currents.
D000200:Action Potentials / Q000187:drug effects; D000547:Amantadine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D004558:Electric Stimulation; D006168:Guinea Pigs; D007473:Ion Channels / Q000187:drug effects*; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D010210:Papillary Muscles / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D011188:Potassium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism
D007473:Ion Channels; C036548:4-bromobenzoyl-methyladamantylamine; D012964:Sodium; D000547:Amantadine; D011188:Potassium; D002118:Calcium