4.5 Article

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

Journal

JOURNAL OF PHARMACOLOGICAL SCIENCES
Volume 133, Issue 4, Pages 195-202

Publisher

JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1016/j.jphs.2016.12.006

Keywords

Pulmonary vein myocardium; Potassium channel; Automaticity; Resting membrane potential; Intracellular Ca2+

Funding

  1. MEXT KAKENHI [JP25860194, JP15K08247]
  2. Pharmaceutical Society of Japan [N-151502]
  3. Grants-in-Aid for Scientific Research [15K08247, 17K15460, 15K07871] Funding Source: KAKEN

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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 (I-K1). 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. (C) 2017 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.

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