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Pacing-Induced Non-Uniform Ca(2+) Dynamics in Rat Atria Revealed by Rapid-Scanning Confocal Microscopy
Intracellular Ca(2+) ([Ca(2+)](i)) dynamics in isolated myocytes differ between the atria and ventricles due to the distinct t-tubular distributions. Although cellular aspects of ventricular [Ca(2+)](i) dynamics in the heart have been extensively studied, little is known about those of atrial myocyt...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4138402/ https://www.ncbi.nlm.nih.gov/pubmed/25221364 http://dx.doi.org/10.1267/ahc.14014 |
Sumario: | Intracellular Ca(2+) ([Ca(2+)](i)) dynamics in isolated myocytes differ between the atria and ventricles due to the distinct t-tubular distributions. Although cellular aspects of ventricular [Ca(2+)](i) dynamics in the heart have been extensively studied, little is known about those of atrial myocytes in situ. Here we visualized precise [Ca(2+)](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 Ca(2+) transients on systole among individual cells, whereas no discernible [Ca(2+)](i) elevation developed during diastole. In contrast, the remaining hearts showed non-uniform [Ca(2+)](i) dynamics within and among the cells especially under high-frequency (4 Hz) excitation, where subcellular cluster-like [Ca(2+)](i) rises or wave-like [Ca(2+)](i) propagation occurred on excitation. Such [Ca(2+)](i) inhomogeneity was more pronounced at high-frequency pacing, showing beat-to-beat Ca(2+) transient alternans. Despite such non-uniform dynamics, cessation of burst pacing of the atria was not followed by emergence of spontaneous Ca(2+) waves, indicating minor Ca(2+)-releasing potentials of the sarcoplasmic reticulum (SR). In summary, rat atria display a propensity to show non-uniform [Ca(2+)](i) dynamics on systole due to impaired Ca(2+)-release from the SR and paucity of t-tubules. Our results provide an important basis for understanding atrial pathophysiology. |
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