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(Circulation Research. 1998;83:1224-1231.)
© 1998 American Heart Association, Inc.

Original Contributions

Quinidine Interactions With Human Atrial Potassium Channels

Developmental Aspects

Neviana I. Nenov, William J. Crumb, Jr, John D. Pigott, Lynn H. Harrison, Jr, Craig W. Clarkson

From the Departments of Pharmacology (N.I.N., C.W.C.), Pediatrics (W.J.C.), and Surgery (J.D.P.), Tulane University School of Medicine, and the Department of Surgery, Louisiana State University School of Medicine (L.H.H.), New Orleans, Louisiana.

Correspondence to Craig W. Clarkson, PhD, Department of Pharmacology SL83, 1430 Tulane Ave, New Orleans, LA 70112-2699. E-mail cclarks{at}tmcpop.tmc.tulane.edu

Abstract—Clinical studies have suggested that quinidine is less effective when used for the treatment of atrial arrhythmias in pediatric patients compared with its clinical effectiveness in the adult patient population. Age-related changes in the cardiac actions of quinidine on action potential duration and interaction with potassium channels in several mammalian species also have been reported. We investigated the effects of postnatal development on quinidine's interaction with major repolarizing currents (I_to, I_Kur, I_ns, and I_K1) in human atrial myocytes, using the whole-cell configuration of the voltage-clamp technique. Our results indicate that there are age-related changes in both the IC₅₀ for quinidine blockade of I_to, as well as the mechanism of quinidine unblocking. In contrast, quinidine was found to inhibit both adult and pediatric I_K1 and I_Kur in an age-independent manner, whereas the nonselective cation current (I_ns), which contributes to the sustained outward current (I_sus), was insensitive to quinidine. The results from this study help to clarify the electrophysiological mechanism by which quinidine elicits its antiarrhythmic effect in the pediatric and adult human population.

Key Words: human • atrial myocyte • development • quinidine • K⁺ channel

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