[Mechanism of outercellular [K+] in generation of pacemaker action potentials in sinoatrial valve of the rabbit]

In a control solution (solution I; 3 mM K+, 35 degrees C) the amplitude of APs of cells in the valve centre was 81 +/- 6 mV (Mean +/- SEM), the maximal upstroke velocity (dV/dtmax) was 19 +/- 4 V/s, velocity slow diastolic depolarization (DD) - 65 +/- 8 mV/s, the rate of spontaneous AP generation was 135 +/- 14 bpm. Hypo K+ (50 %) solution (solution II) decreased slow DD by - 22 % and dV/dtmax by -58 % and the rate of AP generation by 15 % compared to the control solution. In saline solution, decrease of Emax from -68 to -45 mV and four-fold decrease of slow DD and dV/dtmax were registered at the 8th of exposure. After that the Emax noise and origin of early (EADs) and delay (DADs) afterdepolarizations were observed. Comparative analysis of the main AP parameters of SA valve latent pacemaker cells in solution III (without K+) and solution IV (without KC1 and CaCl2) exposure demonstrated that changes of this parameters in solution IV were less then in solution III. It is interesting that in solution IV exposure the phase of the early repolarization (phase 1) was differentiated, dV/dtmax was increased by 21%. The frequency of AP generation decreased by 18 % as in solution with 50% K+. At the same time, EADs were not registered. It seems that the decreasing of the transsarcolemal gradient of K+ depolarized Emax despite Nernst equation. At the same time permeability was decreased for K+ and Na+ ions. That could involve Ca2+ overload and origin of EADs and DADs.