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Modification of subcellular organelles in pressure‐overloaded heart by etomoxir, a carnitine palmitoyltransferase I inhibitor
Author(s) -
Rupp Heinz,
Elimban Vijayan,
Dhalla Naranjan S.
Publication year - 1992
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.6.6.1531968
Subject(s) - pressure overload , medicine , endocrinology , sarcolemma , myosin , chemistry , biology , muscle hypertrophy , biochemistry , myocyte , cardiac hypertrophy
To examine the signals regulating cardiac growth and molecular structure of subcellular organelles, cardiac hypertrophy was induced in rats by constriction of the abdominal aorta for 12–13 wk or by treatment with a carnitine palmitoyltransferase I inhibitor, etomoxir (12–15 mg/kg body wt) for 12–13 wk. In contrast to pressure overload, etomoxir redistributed the myosin isozyme population from V 3 to V 1 and increased the sarcoplasmic reticulum (SR) Ca 2+ ‐stimulated ATPase activity. When rats with pressure‐overloaded hearts were treated with etomoxir, the cardiac hypertrophy was increased whereas the shift in myosin isozymes from V 1 to V 3 was prevented and the depression in SR Ca 2+ ‐stimulated ATPase activity was reversed. Plasma thyroid hormone and insulin concentrations were not altered but triglyceride concentrations were reduced in etomoxir‐treated rats with pressure overload. The data demonstrate a dissociation between cardiac muscle growth and changes in subcellular organelles and indicate that a shift in myocardial substrate utilization may represent an important signal for molecular remodeling of the heart.—Rupp, H.; Elimban, V.; Dhalla, N. S. Modification of subcellular organelles in pressure‐overloaded heart by etomoxir, a carnitine palmitoyltransferase I inhibitor. FASEB J. 6: 2349‐2353; 1992.