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The Na+/Ca2+ exchanger inhibitor SEA0400 significantly reduced the incidence of ouabain-induced electrical activity in guinea-pig pulmonary vein myocardium from 86.7% to 46.7%.
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Pharmacological evidence demonstrates that the Na+/Ca2+ exchanger underlies the automaticity of the pulmonary vein myocardium, providing mechanistic insights relevant to atrial arrhythmogenesis.
We examined the involvement of the Na(+)/Ca(2+) exchanger in the automaticity of the pulmonary vein myocardium with a specific inhibitor, SEA0400. Action potentials were recorded from the myocardial layer of isolated guinea-pig pulmonary vein preparations, and Ca(2+) transients were recorded from the cardiomyocytes. Spontaneous electrical activity was observed in 17.7% of the preparations, which was inhibited by either SEA0400 or ryanodine. In quiescent preparations, ouabain induced electrical activity and spontaneous Ca(2+) transients, which were inhibited by SEA0400, as well as ryanodine. These results provide pharmacological evidence that the Na(+)/Ca(2+) exchanger underlies the automaticity of the pulmonary vein myocardium.
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Namekata et al. (2009) studied Pulmonary vein automaticity (n=141). SEA0400 vs. Vehicle control was evaluated on Incidence of ouabain-induced electrical activity (p=<0.05). The Na+/Ca2+ exchanger inhibitor SEA0400 significantly reduced the incidence of ouabain-induced electrical activity in guinea-pig pulmonary vein myocardium from 86.7% to 46.7%.
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