Role of the Slow Sodium Channel in Hereditary Cardiomyopathy

  • Ghassan Bkaily
  • Gaétan Jasmin
  • Danielle Jacques
  • Libuse Proschek
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 168)


Hereditary cardiomyopathy in the hamster provides unique possibilities for studying the pathology and clinical course of primary congestive cardiomyopathies. The autosomal recessive disorder is readily transmissible with 100% incidence in the offspring, although the defective gene has not yet been identified. The cardiomyopathy develops in a characteristic, well-defined, predictable manner. Verapamil (an L-type Ca2+ blocker) and isoproterenol (an indirect L-type Ca2+ stimulator) were highly efficient in preventing the development of necrotic cardiac changes in the cardiomyopathic hamster (see [1] and references therein). Necrotic changes in cardiomyopathic hamsters become fully expressed at the critical age of 55 days. However, no biochemical or morphological changes were found in the newborn cardiomyopathic hamster. At this stage, early embryonic tetradotoxin (TTX) and Mn2+-insensitive slow sodium channels were detected in the newborn cardiomyopathic hamster [1]. This slow Na+ channel has the same kinetics as the one reported in three-day-old chick embryonic heart cells [2–4]. A similar TTX- and Mn2+-insensitive slow Na+ channel was found in 10- to 19-week-old human fetal heart cells. This early fetal slow Na+ channel was similar in kinetics and pharmacology to the slow Na+ channels in newborn cardiomyopathic heart cells. This type of channel was sensitive to agents that were shown to prevent the development of cardiac necrosis in the cardiomyopathic hamster.


Sodium Channel Syrian Hamster Heart Cell Contractile Dysfunction Ventricular Cell 
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Copyright information

© Kluwer Academic Publishers 1996

Authors and Affiliations

  • Ghassan Bkaily
  • Gaétan Jasmin
  • Danielle Jacques
  • Libuse Proschek

There are no affiliations available

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