Effect of angiotensin-converting enzyme inhibition on protein kinase C and SR proteins in heart failure.
We tested the hypothesis that activation of protein kinase C ( PKC) isoforms in pressure-overload heart failure was prevented by angiotensin-converting enzyme (ACE) inhibition, resulting in normalization of cardiac sarcoplasmic reticulum (SR) Ca2+ ATPase (SERCA) 2a and phospholamban protein levels and improvement in intracellular Ca2+ handling. Aortic-banded and control guinea pigs were given ramipril (5 mg. kg-1. day-1) or placebo for 8 wk. Ramipril-treated banded animals had lower left ventricular (LV) and lung weight, improved survival, increased isovolumic LV mechanics, and improved cardiomyocyte Ca2+ transients compared with placebo-treated banded animals. This was associated with maintenance of SERCA2a and phospholamban protein expression. Translocation of PKC-alpha and -epsilon was increased in placebo-treated banded guinea pigs compared with controls and was attenuated significantly by treatment with ramipril. We conclude that ACE inhibition attenuates PKC translocation and prevents downregulation of Ca2+ cycling protein expression in pressure-overload hypertrophy. This represents a mechanism for the beneficial effects of this therapy on LV function and survival in heart failure.[1]References
- Effect of angiotensin-converting enzyme inhibition on protein kinase C and SR proteins in heart failure. Takeishi, Y., Bhagwat, A., Ball, N.A., Kirkpatrick, D.L., Periasamy, M., Walsh, R.A. Am. J. Physiol. (1999) [Pubmed]
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