Permissive role of reduced inwardly-rectifying potassium current density in the automaticity of the guinea pig pulmonary vein myocardium

• Main Authors: Yayoi Tsuneoka, Masahiko Irie, Yusuke Tanaka, Takahiko Sugimoto, Yuka Kobayashi, Taichi Kusakabe, Keisuke Kato, Shogo Hamaguchi, Iyuki Namekata, Hikaru Tanaka
• Format: Article
• Language: English
• Published: Elsevier 2017-04-01
• Series: Journal of Pharmacological Sciences
• Subjects: Pulmonary vein myocardium; Potassium channel; Automaticity; Resting membrane potential; Intracellular Ca2+
• Online Access: http://www.sciencedirect.com/science/article/pii/S1347861317300427

The electrophysiological properties underlying the automaticity of the guinea pig pulmonary vein myocardium were studied. About 30% of the isolated pulmonary vein tissue preparations showed spontaneous electrical activity, as shown by glass microelectrode recordings from their myocardial layer. The remaining quiescent preparations had a resting membrane potential less negative than that in the left atria. Blockade of the acetylcholine activated potassium current (IK-ACh) by tertiapin induced a depolarizing shift of the resting membrane potential and automatic electrical activity in the pulmonary vein, but not in the atria. The tertiapin-induced electrical activity, as well as the spontaneous activity, was inhibited by the application of carbachol or by chelation of intracellular Ca2+ by BAPTA. The isolated pulmonary vein cardiomyocytes had an IK-ACh density similar to that of the atrial cardiomyocytes, but a lower density of the inwardly-rectifying potassium current (IK1). Spontaneous Ca2+ transients were observed in about 30% of the isolated pulmonary vein cardiomyocytes, but not in atrial cardiomyocytes. The Ca2+ transients in the pulmonary vein cardiomyocytes were induced by tertiapin and inhibited by carbachol. These results indicate that the pulmonary vein cardiomyocytes have a reduced density of the inwardly-rectifying potassium current, which plays a permissive role in their intracellular Ca2+-dependent automaticity.