The aim of the present experiments was to study the characteristics and mechanisms of the rhythm induced by overdrive ('overdrive excitation', ODE) in the sinoatrial node (SAN) superfused in high [K(+)](o) (8-14 mM). It was found that: (1) overdrive may induce excitation in quiescent SAN and during a slow drive; (2) in spontaneously active SAN, overdrive may accelerate the spontaneous discharge; (3) immediately after the end of overdrive, a pause generally precedes the onset of the induced rhythm; (4) during the pause, an oscillatory potential (V(os)) may be superimposed on the early diastolic depolarization (DD); (5) during the subsequent late DD, a different kind of oscillatory potential appears near the threshold for the upstroke (ThV(os)) which is responsible for the initiation of spontaneous activity; (6) once started, the induced rhythm is fastest soon after overdrive; (7) faster drives induce longer and faster spontaneous rhythms; (8) the induced action potentials are slow responses followed by DD with a superimposed V(os), but ThV(os) is responsible for ODE; (9) the induced rhythm subsides when ThV(os) miss the threshold and gradually decay; (10) low [Ca(2+)](o) abolishes ODE; (11) in quiescent SAN, high [Ca(2+)](o) induces spontaneous discharge through ThV(os) and increases its rate by enhancing V(os) and shifting the threshold to more negative values, and (12) tetrodotoxin abolishes ODE as welll as the spontaneous discharge induced by high [Ca(2+)](o). In conclusion, in K(+)-depolarized SAN, ODE may be present in the apparent absence of calcium overload, is Ca(2+)- and Na(+)-dependent and is mediated by ThV(os) and not by V(os). Copyright 1997 S. Karger AG, Basel

The aim of the present experiments was to study the characteristics and mechanisms of the rhythm induced by overdrive (‘overdrive excitation’, ODE) in the sinoatrial node (SAN) superfused in high [K^+](0) (8-14 mM). It was found that; (1) overdrive may induce excitation in quiescent SAN and during a slow drive; (2) in spontaneously active SAN, overdrive may accelerate the spontaneous discharge; (3) immediately after the end of overdrive, a pause generally precedes the onset of the induced rhythm; (4) during the pause, an oscillatory potential (V(os)) may be superimposed on the early diastolic depolarization (DD); (5) during the subsequent late DD, a different kind of oscillatory potential appears near the threshold for the upstroke (ThV(os)) which is responsible for the initiation of spontaneous activity; (6) once started, the induced rhythm is fastest soon after overdrive; (7) faster drives induce longer and faster spontaneous rhythms; (8) the induced action potentials are slow responses followed by DD with a superimposed Vos, but ThV(os) is responsible for ODE; (9) the induced rhythm subsides when ThV(os) miss the threshold and gradually decay; (10) low [Ca^2+](0) abolishes ODE; (11) in quiescent SAN, high [Ca^2+](0) induces spontaneous discharge through ThV(os) and increases its rate by enhancing V(os) and shifting the threshold to more negative values, and (12) tetrodotoxin abolishes ODE as well as the spontaneous discharge induced by high [Ca^2+](0). In conclusion, in K^+-depolarized SAN, ODE may be present in the apparent absence of calcium overload, is Ca^2+- and Na^+-dependent and is mediated by ThV(os) and not by V(os).