An adamantane derivative (N-N' (1-adamantil) -ethylene diamine dibromide) induced automaticity in the ventricular myocardium of the frog
Mészáros, J.; Kovács, T.; Dinya, A.; Szegi, J.
Acta Physiologica Academiae Scientiarum Hungaricae 58(1): 79-87
1981
ISSN/ISBN: 0001-6756 PMID: 6979163 Document Number: 177970
The effect of an adamantane derivative (N,N'(1-adamantyl)-ethylenediamine dibromide; AED) on the transmembrane potentials and contractile activity of isolated electrically driven frog ventricular strips were studied. The effect of AED on the 42K efflux in ventricular muscle rings was also investigated. AED at a concentration of 10-3 M markedly reduced the rate of depolarization and prolonged the duration of action potential. The resting potential was shifted to less negative potential ranges and pacemaker-like action potentials appeared within 10 min of exposure to drug. AED was found to exert an enhancing effect on the contractile force of the frog ventricular muscle. The slow Ca2+-channel blocker D-600 was able to abolish completely the AED-induced automaticity, while the .beta.-adrenoceptor blocker pindolol failed to prevent this action. The pacemaker activity was reduced by increasing external K+ concentration. AED markedly reduced the 42K efflux in ventricular muscle rings. The AED induced automaticity by decreasing the outward movement of K+ ions and by depolarizing the cell membrane.