Difference in Propagation of Ca〔2+〕 Release in Atrial and Ventricular Myocytes

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  • Tanaami Takeo
    Bio Technology Laboratory, R&D Center, Yokogawa Electric Corporation
  • Ishida Hideyuki
    Department of Physiology, School of Medicine, Tokai University
  • Seguchi Hidetaka
    Division of Cardiology, University of Utah Health Sciences Center
  • Hirota Yuki
    Department of Physiology, School of Medicine, Tokai University
  • Kadono Toshie
    Division of Cardiology, University of Utah Health Sciences Center
  • Genka Chokoh
    Department of Physiology, School of Medicine, Tokai University
  • Nakazawa Hiroe
    Department of Physiology, School of Medicine, Tokai University
  • H. Barry William
    Division of Cardiology, University of Utah Health Sciences Center

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  • Difference in Propagation of Ca2+ Release in Atrial and Ventricular Myocytes

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Intracellular [Ca2+] ([Ca2+]i) was imaged in atrial and ventricular rat myocytes by means of a high-speed Nipkow confocal microscope. Atrial myocytes with an absent t-tubule system on 8-di- ANEPPS staining showed an initial rise in Ca2+ at the periphery of the cell, which propagated to the interior of the cell. Ventricular myocytes showed a uniform rise in [Ca2+]i after electrical stimulation, consistent with a prominent t-tubular network. In atrial myocytes, there was a much shorter time between the peak of the [Ca2+]i transient and the peak contraction as compared to ventricular myocytes. A regional release of Ca2+ induced by an exposure of one end of the myocyte to caffeine with a rapid solution switcher resulted in a uniform propagation of Ca2+ down the length of the cell in atrial myocytes, but we found no propagation in ventricular myocytes. A staining with rhodamine 123 indicated a much greater density of mitochondria in ventricular myocytes than in atrial myocytes. Thus the atrial myocytes display a lack of “local control” of Ca2+ release, with propagation after the Ca2+ release at the periphery induced by stimulation or at one end of the cell induced by exposure to caffeine. Ventricular myocytes showed the presence of local control, as indicated by an absence of the propagation of a local caffeine-induced Ca2+ transient. We suggest that this finding, as well as a reduced delay between the peak of the [Ca2+]i transient and the peak shortening in atrial myocytes, could be due in part to reduced Ca2+ buffering provided by mitochondria in atrial myocytes as opposed to ventricular myocytes.<br>

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