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1 Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6; and 2 Aoto Hospital, Jikei University, Tokyo 125-8506, Japan
The
activities of cardiac protein kinase C (PKC) were examined in
hemodynamically assessed rats subsequent to myocardial infarction (MI).
Both Ca2+-dependent and Ca2+-independent PKC
activities increased significantly in left ventricular (LV) and right
ventricular (RV) homogenates at 1, 2, 4, and 8 wk after MI was induced.
PKC activities were also increased in both LV and RV cytosolic and
particulate fractions from 8-wk infarcted rats. The relative protein
contents of PKC-
, -
, -
, and -
isozymes were significantly
increased in LV homogenate, cytosolic (except PKC-), and particulate
fractions from the failing rats. On the other hand, the protein
contents of PKC-, -, and - isozymes, unlike the PKC-
isozyme, were increased in RV homogenate and cytosolic fractions,
whereas the RV particulate fraction showed an increase in the PKC-
isozyme only. These changes in the LV and RV PKC activities and protein
contents in the 8-wk infarcted animals were partially corrected by
treatment with the angiotensin-converting enzyme inhibitor imidapril.
No changes in protein kinase A activity and its protein content were
seen in the 8-wk infarcted hearts. The results suggest that the
increased PKC activity in cardiac dysfunction due to MI may be
associated with an increase in the expression of PKC-, -, and
- isozymes, and the improvement of heart function in the infarcted
animals by imidapril may be due to partial prevention of changes in PKC
activity and isozyme contents.
protein kinase A; angiotensin-converting enzyme inhibitor; isozymes
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