Pacing-Induced Non-Uniform Ca<sup>2+</sup> Dynamics in Rat Atria Revealed by Rapid-Scanning Confocal Microscopy

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  • Jiang Yan
    Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Graduate School of Medical Science
  • Tanaka Hideo
    Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Graduate School of Medical Science
  • Matsuyama Taka-aki
    Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Graduate School of Medical Science Department of Pathology, National Cerebral and Cardiovascular Center
  • Yamaoka Yoshihisa
    Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Graduate School of Medical Science
  • Takamatsu Tetsuro
    Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Graduate School of Medical Science

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Abstract

Intracellular Ca2+ ([Ca2+]i) dynamics in isolated myocytes differ between the atria and ventricles due to the distinct t-tubular distributions. Although cellular aspects of ventricular [Ca2+]i dynamics in the heart have been extensively studied, little is known about those of atrial myocytes in situ. Here we visualized precise [Ca2+]i dynamics of atrial myocytes in Langendorff-perfused rat hearts by rapid-scanning confocal microscopy. Of 16 fluo-4-loaded hearts imaged during pacing up to 4-Hz, five hearts showed spatially uniform Ca2+ transients on systole among individual cells, whereas no discernible [Ca2+]i elevation developed during diastole. In contrast, the remaining hearts showed non-uniform [Ca2+]i dynamics within and among the cells especially under high-frequency (4 Hz) excitation, where subcellular cluster-like [Ca2+]i rises or wave-like [Ca2+]i propagation occurred on excitation. Such [Ca2+]i inhomogeneity was more pronounced at high-frequency pacing, showing beat-to-beat Ca2+ transient alternans. Despite such non-uniform dynamics, cessation of burst pacing of the atria was not followed by emergence of spontaneous Ca2+ waves, indicating minor Ca2+-releasing potentials of the sarcoplasmic reticulum (SR). In summary, rat atria display a propensity to show non-uniform [Ca2+]i dynamics on systole due to impaired Ca2+-release from the SR and paucity of t-tubules. Our results provide an important basis for understanding atrial pathophysiology.

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