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Updated: Aug 7, 2026
Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
Published on: July 5, 2021
On the mechanisms underlying diastolic voltage oscillations in the sinoatrial node
John N Catanzaro1, Michael P Nett, Marcello Rota
1Department of Physiology and Pharmacology, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA.
Aim:
The study of the mechanisms underlying the oscillatory afterpotential (V(os)) and prepotential (ThV(os)).
Background:
It has been recently shown that V(os) and ThV(os) play an obligatory role in the dominant sinoatrial node (SAN) discharge.
Methods:
Guinea pig isolated SAN was studied in vitro by means of a microelectrode technique.
Results:
High [K(+)](o) and premature stimuli unmask V(os) superimposed on early diastolic depolarization and ThV(os) within a less negative voltage range ("oscillatory zone"). Subthreshold stimuli elicit ThV(os) in the oscillatory zone, but not at more negative values. Drive and caffeine shift the oscillatory zone in a negative direction. Low caffeine concentrations increase the size of V(os) and of ThV(os), rate, and force. High caffeine concentrations suppress V(os) but increase the size of ThV(os) and shift them to more negative values until they eventually miss the threshold. In quiescent SAN in high caffeine, a fast drive enhances ThV(os) size, thereby initiating a transient spontaneous rhythm ("overdrive excitation"). Adrenergic agonists potentiate caffeine-induced overdrive excitation through an increase in ThV(os). In high caffeine, the first twitch after quiescence is not larger, twitch relaxation is slower, V(os) is abolished, and the prolonged nonoscillatory afterdepolarization V(ex) is induced, consistent with an impairment of Ca2+ handling by the sarcoplasmic reticulum. The effects of caffeine in Tyrode's solution are accounted for by the caffeine-induced changes in the oscillatory potentials. Tetrodotoxin decreases force and size of both V(os) and ThV(os).
Conclusions:
The mechanism underlying V(os) is related to a diastolic release of Ca2+ from a Ca2+-overloaded sarcoplasmic reticulum, whereas that of ThV(os) appears to be related to ionic currents in the resting potential range that can initiate and sustain spontaneous discharge.
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