Key result
Vagal stimulation reduces sinoatrial space constants ~14% and diminishes electrotonic potential via decreased membrane resistance.
Vagal stimulation decreases membrane resistance and electrotonic interaction within the sinoatrial node, which may impact electrical synchronization of nodal fibers.
May alter sinoatrial synchronization; leaves open arrhythmia relevance pending in vivo human studies.
OBJECTIVE: The effect of vagal stimulation on the decay of electrotonic potential caused by intracellular current injection and on input resistance was measured in the sinoatrial node of isolated rabbit right atria. METHODS: Studies were performed on New Zealand White rabbits weighing approximately 2-3 kg. Vagal stimulation was achieved by transmural stimulation of intramural nerve fibres in the presence of propranolol. A K+ perfused suction electrode was used to inject hyperpolarising current pulses; input resistance was measured by means of a double barrel microelectrode. RESULTS: Vagal stimulation which caused a 14-20% increase of cycle length diminished electronic potential significantly by a decrease of membrane resistance. The input resistance of the sinoatrial node was not affected. Space constant values calculated by using either a one or a two dimensional model of electrotonic current spread were decreased on average by 13% and 14% respectively. CONCLUSIONS: The results from this study show that vagal stimulation which gave rise to a moderate negative chronotropic effect and marked changes in action potential configuration of nodal fibres affects the electrotonic interaction within the sinoatrial node. This may have consequences for the electrical activity and synchronisation of the sinoatrial nodal fibres.
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Duivenvoorden et al. (1992) studied this question. Transmural vagal stimulation was evaluated on Decay of electrotonic potential and input resistance. Vagal stimulation decreased space constant values by 13-14% and diminished electrotonic potential via decreased membrane resistance, without affecting input resistance of the sinoatrial node.
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