title: [Slow activated voltage-dependent sodium current contribution in fast depolarization in the rabbit heart true pacemaker sinoatrial node].
abstract: The functional role of INa in initiation and conduction of cardiac true pacemaker activity remains uncertain. Therefore the goal of this work was to study the effects of Na+ substitution of action potentials parameters of the sinoatrial area cells. Transmembrane action potentials were recorded with 15 to 40 MOmega glass microelectrodes filled with 2.5 M KCl. The final preparations was about 5 x 3 mm in size, contained a portion sinoatrial node and the adjacent fragment of tissue of the right branch of the sinoatrial ring bundle and crista terminalis. All strips were allowed to beat spontaneously. We have registered that Na+ replacement of 50% in external solution causes an almost two-fold monotonous decrease of dV/dtmax and overshoot values of primary (3.2 V/s, n = 15), latent pacemaker (17 V/s, n = 16) and "conducting"-like cells (130 V/s, n = 16, control, 35 C) as compared with the control. Finally (at 30 min exposure) action potential frequency is slowed dowb by 20-30%. True pacemaker cells decreased action potential amplitude from 65 to 9 mV for 20-30 min 50% Na solution exposure. It should be noted that the cells of the "conducting"-like type demonstrated the generation block of action potential 30% Na exposure. At the same time dV/dtmax monotonously decreased from 3.1 to 1.5 V/s (true pacemaker) 16 vs 7 V/s (latent) and from 130 to 1.8 v/s ("conducting"). In our opinion, these facts deserve particular attention because it has been reported earlier that tetrodotoxin (20 mcM) addition in to the control solution caused the decrease of dV/dt from 100 to 4 V/s in latent pacemaker, whereas action potential amplitude is decreased by only some mV and the rate of beating by 1.5 times. As for true pacemaker cells, the TTX does not influence them.
authors.forename: V A
authors.initials: VA
authors.lastname: Golovko
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology*; D006329:Heart Conduction System / Q000187:drug effects / Q000502:physiology*; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D008297:Male; D011817:Rabbits; D012849:Sinoatrial Node / Q000187:drug effects / Q000502:physiology*; D012964:Sodium / Q000502:physiology*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D026941:Sodium Channel Blockers; D015222:Sodium Channels; D013779:Tetrodotoxin; D012964:Sodium