• Han Choe, Yu-Kyung Lee, Yong-Tae Lee, Huhn Choe, Seong-Hoon Ko, Chan-Uhng Joo, Min-Ho Kim, Gong-Soo Kim, Jae-Soon Eun, Jong-Hyun Kim, Soo-Wan Chae, and Yong-Geun Kwak.
• Department of Physiology, Ulsan University College of Medicine, Seoul, South Korea.
• J. Pharmacol. Exp. Ther. 2003 Feb 1;304(2):706-12.

AbstractPapaverine, 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 IC(50) value of 43.4 microM at +60 mV. Papaverine accelerated the kinetics of the channel inactivation, suggesting the blockade of open channels. Papaverine (100 microM) 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.

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