Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Satoh, H.

Satoh,

Comparative actions of cibenzoline and disopyramide on I(Kr) and I(Ks) currents in rat sino-atrial nodal cells.

Modulation by class Ia antiarrhythmic drugs, cibenzoline and disopyramide, of the pacemaking activity and the underlying ionic currents in rat sino-atrial nodal cells was investigated using current-clamp and whole-cell patch-clamp techniques. Both drugs depressed the spontaneous activity and often caused sinus arrest. The negative chronotropic effect was significant at 10 microM cibenzoline and 30 microM disopyramide. The L-type Ca(2+) current (I(Ca)) and the hyperpolarization-activated inward current decreased by 69.7+/-3.2% and by 45.8+/-3.0% at 30 microM cibenzoline and by 51. 2+/-3.3% and by 48.3+/-2.7% at 100 microM disopyramide, respectively. The delayed rectifier K(+) current, which is composed of rapidly and slowly activated currents (I(Kr) and I(Ks)), also decreased. The IC(50) values of I(Kr) for cibenzoline and disopyramide were 8.8+/-1. 1 and 25.1+/-2.3 microM, respectively. In the presence of 5 microM E-4031 (1-[2-(6-methyl-2-pyridyl)ethyl]-4-(4-methylsulfonylaminobenzoyl) piperidine), the IC(50) values of I(Ks) for cibenzoline and disopyramide were 12.3+/-1.8 and 81.1+/-2.3 microM, respectively. The I(Ks) was completely blocked by 30 microM 293B (trans-6-cyano-4-(N-ethylsulphonyl-N-methtamino)-3-hydroxy-2 , 2-dimethyl-chromane). These results indicate that the ionic currents are more sensitive to cibenzoline than disopyramide in rat sino-atrial nodal cells, and that I(Ca) and I(Kr) make major contributions to pacemaking activity.[1]

References

Comparative actions of cibenzoline and disopyramide on I(Kr) and I(Ks) currents in rat sino-atrial nodal cells. Satoh, H. Eur. J. Pharmacol. (2000) [Pubmed]

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