Potassium channel activators differentially modulate the effect of sodium channel blockade on cardiac conduction.

ABSTRACT:

Aims

Diminished repolarization reserve contributes to the arrhythmogenic substrate in many disease states. Pharmacological activation of K(+) channels has been suggested as a potential antiarrhythmic therapy in such conditions. Having previously demonstrated that I(K1) and I(Kr) can modulate cardiac conduction, we tested here the effects of pharmacological I(KATP) and I(Ks) activation on cardiac conduction and its dependence on the sodium current (I(Na)).

Methods and results

Bath electrocardiograms (ECGs) recorded from Langendorff-perfused guinea pig ventricles revealed QRS prolongation during I(KATP) activation by pinacidil but not during I(Ks) activation by R-L3 relative to control. In contrast, when I(Na) was partially blocked by flecainide, R-L3 but not pinacidil prolong

SUBMITTER: Veeraraghavan R 

PROVIDER: S-EPMC3980511 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature