Abstract
The present study investigated the influence of overexpression of the cardiac Na+-Ca2+exchanger on myocardial force of contraction and alterations in sarcoplasmic reticulum (SR) Ca2+-handling proteins in a transgenic mouse model. Inotropic effects of Na+channel agonist BDF 9148 and isoprenaline were determined in isolated electrically driven atria. Protein levels of key SR Ca2+-handling proteins were determined by Western blot analysis. Transgenic animals had no myocardial hypertrophy or failure. The positive inotropic effect of BDF 9148 was significantly more pronounced in myocardium from transgenic animals, whereas the inotropic response to isoprenaline was similar in both groups. Strong immunoreactivity of the transgene Na+-Ca2+exchanger was detected in myocardium of transgenic animals. Protein levels of SR Ca2+-ATPase, phospholamban, and calsequestrin were unchanged. In conclusion, transgenic overexpression of the Na+-Ca2+exchanger is accompanied by increased force development following Na+channel agonist administration, even though Ca2+proteins of the SR are unchanged.
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