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Am J Physiol Cell Physiol (June 30, 2004). doi:10.1152/ajpcell.00155.2004
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Submitted on March 24, 2004
Accepted on June 4, 2004

Cardiac Contractile Dysfunction in J2N-k Cardiomyopathic Hamsters is Associated with Impaired Function and Regulation of the Sarcoplasmic Reticulum

Andrea P Babick1, Elliott J Cantor1, John T Babick1, Nobuakira Takeda2, Naranjan S Dhalla1, and Thomas Netticadan1*

1 Physiology, Institute of Cardiovascular Sciences/University of Manitoba, Winnipeg, Manitoba, Canada
2 General Medicine, Aoto Hospital/Jikei University School of Medicine, Katsushika-ku, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: tnetticadan{at}sbrc.ca.

Although dilated cardiomyopathy (DCM) is known to result in cardiac contractile dysfunction, the underlying mechanisms are unclear. The sarcoplasmic reticulum (SR) is the main regulator of intracellular Ca2+ required for cardiac contraction and relaxation. We therefore hypothesized that abnormalities in both SR function and its regulation will contribute to cardiac contractile dysfunction of the J2N-k cardiomyopathic hamster, an appropriate model of DCM. Echocardiographic assessment indicated contractile dysfunction, as the ejection fraction, fractional shortening, cardiac output and heart rate were all significantly reduced in J2N-k hamsters as compared to controls. Depressed cardiac function was associated with decreased cardiac SR Ca2+-uptake in the cardiomyopathic hamsters. Reduced SR Ca2+-uptake could be further linked to a decrease in the expression of the sarcoendoplasmic reticulum ATPase and cAMP-dependent protein kinase (PKA) mediated phospholamban (PLB) phosphorylation at serine-16. Depressed PLB phosphorylation was paralleled with a reduction in the activity of SR-associated PKA, as well as an elevation in protein phosphatase activity in J2N-k hamster. The results of this study suggest that an alteration in SR function and its regulation contribute to cardiac contractile dysfunction in the J2N-k cardiomyopathic hamster.




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