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CARDIOVASCULAR

Papaverine Blocks hKv1.5 Channel Current and Human Atrial Ultrarapid Delayed Rectifier K⁺ Currents

Department of Physiology, Ulsan University College of Medicine, Seoul, South Korea (Ha.C.); Departments of Pharmacology (Y.-K.L. Y.-T.L., J.-H.K., S.-W.C., Y.-G.K.), Anesthesiology (Hu.C., S.-H.K.), Pediatrics (C.-U.J. and M.-H.K.), and Thoracic and Cardiovascular Surgery (G.-S.K.), and Institute of Cardiovascular Research (S.-W.C., Y.-G.K.), Chonbuk National University Medical School, Chonju, South Korea; and Departments of Pharmacology, Woosuk University College of Pharmacy, Wanju, South Korea (J.-S.E.)

Papaverine, 1-[(3,4-dimethoxyphenyl)methyl]-6,-7-dimethoxyisoquinoline, has been used as a vasodilator agent and a therapeutic agent for cerebral vasospasm, renal colic, and penile impotence. We examined the effects of papaverine on a rapidly activating delayed rectifier K⁺ channel (hKv1.5) cloned from human heart and stably expressed in Ltk^– cells as well as a corresponding K⁺ current (the ultrarapid delayed rectifier, I_Kur) in human atrial myocytes. Using the whole cell configuration of the patch-clamp technique, we found that papaverine inhibited hKv1.5 current in a time-and voltage-dependent manner with an IC₅₀ value of 43.4 µM at +60 mV. Papaverine accelerated the kinetics of the channel inactivation, suggesting the blockade of open channels. Papaverine (100 µM) also blocked I_Kur in human atrial myocytes. These results indicate that papaverine blocks hKv1.5 channels and native hKv1.5 channels in a concentration-, voltage-, state-, and time-dependent manner. This interaction suggests that papaverine could alter cardiac excitability in vivo.

Address correspondence to: Dr. Yong-Geun Kwak, Department of Pharmacology, Chonbuk National University Medical School, Chonju, Chonbuk 561-180, South Korea. E-mail: ygkwak{at}moak.chonbuk.ac.kr

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