Intracellular calcium and membrane potential oscillations in the pulmonary vein myocardium

[Speaker] Iyuki Namekata:1
[Co-author] Masahiko Iie:1, Haruna Kanae:1, Yayoi Tsuneoka:1, Shogo Hamaguchi:1, Hikaru Tanaka:1
1:Department of Pharmacology, Toho University, Faculty of Pharmaceutical Sciences, Japan

Myocardial intracellular Ca2+ and membrane potential oscillations were studied in the isolated guinea-pig, rat and mouse pulmonary veins with immunohistochemical, confocal microscopic and electrophysiological analyses. The myocardial layer was present between the smooth muscle layer and the adventitia. Intracellular Ca2+ oscillations were observed in three species, which were inhibited by ryanodine. Spontaneous Ca2+ waves were observed to propagate along the longitudinal axis of the cell or as a spiral rotating around a subcellular core; the propagation velocity of these Ca2+ waves was similar to that reported in atrial and ventricular cardiomyocytes. In quiescent pulmonary vein cardiomyocytes, membrane transporter inhibitors such as ouabain, tertiapin and ATX-2 induced Ca2+ oscillations and repetitive Ca2+ transients. Spontaneous action potentials were present in about 35%, 4% 45% of the preparations from the guinea-pig, rat and mouse respectively. In quiescent preparations from the guinea-pig, noradrenaline induced a slow depolarization of the resting membrane potential followed by constant repetitive generation of action potentials, which were inhibited by ryanodine. In quiescent preparations from the rat, noradrenaline induced an initial hyperpolarization and a subsequent depolarization of the resting membrane potential. This was followed by generation of automatic action potentials which occurred in repetitive bursts with a similar maximum diastolic potential during and between bursts. Ryanodine either abolished or reduced the duration of action-potential bursts. In quiescent preparations from the mouse, noradrenaline induced automatic electrical activity which appeared in the three waveform types; the first was a constant firing (like guinea-pig type) and the second was a repetitive burst (like rat type) and the third was also a repetitive burst but with a more negative maximum diastolic potential between the bursts than during the bursts and thus an EAD-like waveform. These results indicate that the pulmonary vein myocardium generates automatic electrical activity under adrenergic influence, which is probably triggered by intracellular Ca2+ oscillations. The difference in firing pattern between the guinea-pig, rat and mouse may be due to the difference in hyperpolarizing mechanisms.
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