 | HEART IN STRESS
Copyright © 1999 by the New York Academy of Sciences
description
Annals of the New York Academy of Sciences 874:100-110 (1999)
© 1999 New York Academy of Sciences
Subcellular Remodeling and Heart Dysfunction in Cardiac Hypertrophy due to Pressure Overloada
NARANJAN S. DHALLAb,
LEONARD GOLFMAN,
XUELIANG LIU,
HIDEKI SASAKI,
VIJAYAN ELIMBAN AND
HEINZ RUPP
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnepeg, Manitoba R2H 2A6 Canada
Department of Physiology, Faculty of Medicine,University of Manitoba,Winnipeg, Manitoba R2H 2A6, Canada
aThe research reported in this article was supported by a grant from the Medical Research Council of Canada (MRC Group in Experimental Cardiology). H.R., a Visiting Professor from University of Marburg, Marburg, Germany, was supported by the NATO Research Program (0189/87) and the Science & Technology Cooperation Germany/Canada (HM4).
bAddress correspondence to: Dr. Naranjan S. Dhalla, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, 351 Tache Avenue, Winnipeg, Manitoba R2H 2A6, Canada.
Rats were treated with etomoxir, an inhibitor of palmitoyltransferase-1, to examine the role of a shift in myocardial metabolism in cardiac hypertrophy. Pressure overload was induced by abdominal aorta banding for 8 weeks. Sham-operated animals served as control. Left ventricular dysfunction, as reflected by decreased LVDP, +dP/dt, -dP/dt, and elevated LVEDP in the pressure overloaded animals, was improved by treatment with etomoxir. Cardiac hypertrophy in pressure-overload rats decreased the sarcoplasmic reticular (SR) Ca 2+ uptake and Ca 2+ release as well as myofibrillar Ca 2+-stimulated ATPase and myosin Ca 2+-ATPase activities; these changes were attenuated by treatment with etomoxir. Steady-state mRNA levels for  - and ß-myosin heavy chains, SR Ca 2+-pump, and protein content of SR Ca 2+-pump were reduced in hypertrophied hearts; these alterations were prevented by etomoxir treatment. The results indicate that modification of changes in myocardial metabolism by etomoxir may prevent remodeling of myofibrils and SR membrane and thereby improve cardiac function in hypertrophied heart.
This article has been cited by other articles:
|
|
|
|
 
R. Sethi, H. K. Saini, X. Guo, X. Wang, V. Elimban, and N. S. Dhalla
Dependence of changes in beta-adrenoceptor signal transduction on type and stage of cardiac hypertrophy
J Appl Physiol,
March 1, 2007;
102(3):
978 - 984.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Sathish, A. Xu, M. Karmazyn, S. M. Sims, and N. Narayanan
Mechanistic basis of differences in Ca2+-handling properties of sarcoplasmic reticulum in right and left ventricles of normal rat myocardium
Am J Physiol Heart Circ Physiol,
July 1, 2006;
291(1):
H88 - H96.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. L. Dries, N. K. Sweitzer, M. H. Drazner, L. W. Stevenson, and B. J. Gersh
Prognostic impact of diabetes mellitus in patients with heart failure according to the etiology of left ventricular systolic dysfunction
J. Am. Coll. Cardiol.,
August 1, 2001;
38(2):
421 - 428.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
