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Background  The diastolic oscillatory after-potential V os  and pre-potential ThV os  play an essential role in the pacemaker mechanism of sino-atrial node (SAN). The aim of this study was to investigate whether these oscillatory potentials are also involved in adrenergic control of SAN discharge.    Methods  V os  and ThV os  were visualized by superfusing guinea pig SAN in high [K + ] o . The actions of adrenergic agonists on oscillatory potentials were studied by means of a microelectrode technique. Statistical significance was determined by means of Student's paired  t -test.    Results  In non-spontaneous SAN, norepinephrine (NE) decreased the resting potential into a voltage range ("oscillatory zone") where increasingly larger ThV os  appeared and initiated spontaneous discharge. In slowly discharging SAN, NE gradually increased the rate by increasing the amplitude and slope of earlier-occurring ThV os  and of V os  until these oscillations fused with initial diastolic depolarization (DD 1 ). In the presence of NE, sudden fast rhythms were initiated by large V os  that entered a more negative oscillatory zone and initiated a large ThV os . Recovery from NE exposure involved the converse changes. The β-adrenergic agonist isoproterenol had similar actions. Increasing calcium load by decreasing high [K + ] o , by fast drive or by recovery in Tyrode solution led to growth of V os  and ThV os  which abruptly fused when a fast sudden rhythm was induced. Low [Ca 2+ ] o  antagonized the adrenergic actions. Cesium (a blocker of I f ) induced spontaneous discharge in quiescent SAN through ThV os . In spontaneous SAN, Cs + increased V os  and ThV os , thereby increasing the rate. Cs +  did not hinder the positive chronotropic action of NE. Barium increased the rate, as Cs +  did.    Conclusion  Adrenergic agonists: (i) initiate SAN discharge by decreasing the resting potential and inducing ThV os ; (ii) gradually accelerate SAN rate by predominantly increasing size and slope of earlier and more negative ThV os ; (iii) can induce sudden fast rhythms through the abrupt fusion of large V os  with large ThV os ; (iv) increase V os  and ThV os by increasing cellular calcium; and (v) do not modify the oscillatory potentials by means of the hyperpolarization-activated current I f . The results provide evidence for novel mechanisms by which the SAN dominant pacemaker activity is initiated and enhanced by adrenergic agonists.

Essential role of diastolic oscillatory potentials in adrenergic control of guinea pig sino-atrial node discharge