Human Atrial Natriuretic Peptide Suppresses Torsades de Pointes in Rabbits

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Background The increase in inward current, primarily L-type Ca^<2+> current, facilitates torsades de pointes (TdP). Because human atrial natriuretic peptide (ANP) moderates the L-type Ca^<2+> current, in our study it was hypothesized that ANP counteracts TdP. Methods and Results We tested the effect of ANP, guanosine 3', 5'-cyclic monophosphate analogue (8-bromo cGMP) and hydralazine on the occurrence of TdP in a rabbit model. In control rabbits, administration of methox-amine and nifekalant almost invariably caused TdP (14/15). In contrast, ANP (10μg・kg^<-1>・min^<-1>) markedly abolished TdP (2/15), whereas hydralazine failed to show a comparable anti-arrhythmic action (10/15). TdP occurred only in 1 of 15 rabbits treated with 8-bromo cGMP. Presence of early afterdepolarization-like hump in the ventricular monophasic action potential was associated with the occurrence of TdP. Conclusion Results suggest that ANP affects TdP in the rabbit model, and that this anti-arrhythmic effect of ANP is not necessarily shared by other vasodilating agents.
2008-04-20