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Calcium currents in postinfarction rat cardiac myocytes
X Q Zhang1, R L Moore, D L Tillotson
1Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033, USA.
The American Journal of Physiology
|December 1, 1995
Summary
Myocytes from rat hearts after myocardial infarction (MI) show reduced calcium levels during contraction, not due to less calcium entry via L-type channels. Beta-adrenergic response is impaired in MI myocytes.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
- Cardiac Pathophysiology
Background:
- Myocardial infarction (MI) in rats leads to reduced peak cytosolic calcium concentration ([Ca2+]i) in myocytes.
- This reduction is exacerbated by isoproterenol or elevated extracellular calcium ([Ca2+]o).
Purpose of the Study:
- To investigate if reduced [Ca2+]i in MI myocytes is caused by diminished calcium entry.
- To assess the function of L-type calcium channels and beta-adrenergic signaling post-MI.
Main Methods:
- Isolated rat myocytes from MI and Sham groups were studied 3 weeks post-surgery.
- Dihydropyridine (DHP) binding and whole-cell calcium current (ICa) were measured.
- Effects of isoproterenol and forskolin on ICa were evaluated.
Main Results:
- DHP binding was reduced in MI myocytes, but whole-cell ICa did not differ significantly between Sham and MI groups at physiological [Ca2+]o.
- Isoproterenol failed to increase ICa in MI myocytes, unlike in Sham myocytes.
- Forskolin effectively increased ICa in MI myocytes, indicating normal adenylate cyclase-protein kinase A signaling.
Conclusions:
- Reduced systolic [Ca2+]i in MI myocytes is not due to decreased L-type calcium channel entry.
- Altered G protein coupling, not channel dysfunction, likely underlies the blunted beta-adrenergic response in MI.
- Discrepancies in DHP binding and ICa suggest changes in channel gating or availability post-MI.