Flecainide blocks the stimulatory effect of veratridine on slowly adapting pulmonary stretch receptors in anaesthetized rabbits without changing lung mechanics.
We examined the responses of slowly adapting pulmonary stretch receptors (PSRs), total lung resistance (RL) and dynamic lung compliance (Cdyn) to administered veratridine before and after pretreatment with atropine or flecainide in anaesthetized, artificially ventilated rabbits with bilateral vagotomy. Administration of veratridine (10 and 30 micrograms kg-1) caused vigorous stimulation of PSRs, resulting in a tonic discharge of receptors during both inflation and deflation, but did not significantly alter either RL or Cdyn. The veratridine-induced PSR stimulation became more prominent, as the dose of this alkaloid was increased. Pretreatment with atropine (1 or 2 mg kg-1) had no significant effect on the excitatory response of PSRs to veratridine. The veratridine-induced PSR stimulation was inhibited by treatment with flecainide (1, 2 and 3 mg kg-1), a sodium channel blocker, and this inhibition was dose-dependent. These results suggest that activation of PSRs following veratridine administration probably related to the increased influx of sodium ions into the receptive terminals but does not depend upon bronchoconstriction.[1]References
- Flecainide blocks the stimulatory effect of veratridine on slowly adapting pulmonary stretch receptors in anaesthetized rabbits without changing lung mechanics. Matsumoto, S., Shimizu, T. Acta Physiol. Scand. (1995) [Pubmed]
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