Essential role of diastolic oscillatory potentialsin adrenergic control of guinea pig sino-atrial node discharge
The diastolic oscillatory after-potential Vos and pre-potential ThVos 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: Vos and ThVos 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 ThVos appeared and initiated spontaneous discharge.
In slowly discharging SAN, NE gradually increased the rate by increasing the amplitude and slope of earlier-occurring ThVos and of Vos until these oscillations fused with initial diastolic depolarization (DD1). In the presence of NE, sudden fast rhythms were initiated by large Vos that entered a more negative oscillatory zone and initiated a large ThVos.
Recovery from NE exposure involved the converse changes. The beta-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 Vos and ThVos which abruptly fused when a fast sudden rhythm was induced. Low [Ca2+]o antagonized the adrenergic actions.
Cesium (a blocker of If) induced spontaneous discharge in quiescent SAN through ThVos. In spontaneous SAN, Cs+ increased Vos and ThVos, thereby increasing the rate.
Cs+ did not hinder the positive chronotropic action of NE. Barium increased the rate, as Cs+ did.
Conclusions: Adrenergic agonists: (i) initiate SAN discharge by decreasing the resting potential and inducing ThVos; (ii) gradually accelerate SAN rate by predominantly increasing size and slope of earlier and more negative ThVos; (iii) can induce sudden fast rhythms through the abrupt fusion of large Vos with large ThVos; (iv) increase Vos and ThVos by increasing cellular calcium; and (v) do not modify the oscillatory potentials by means of the hyperpolarization-activated current If.
The results provide evidence for novel mechanisms by which the SAN dominant pacemaker activity is initiated and enhanced by adrenergic agonists.
Author: Mario VassalleJohn CatanzaroMichael NettMarcello Rota
Credits/Source: Journal of Biomedical Science 2009, 16:101
Published on: 2009-11-18
Copyright by the authors listed above - made available via BioMedCentral (Open Access). Please
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