Calpain is activated during hypoxic myocardial cell injury.
Cell death during hypoxia rose to 80% after 6 h. Calpain activity increased to 4 units during hypoxia, much higher than the 0.7 units seen in aerobic condition at 6 h. This activity was markedly inhibited by calpain-specific inhibitor I (n-acetyl-leucyle-leucyle-norleucinal). beta-Adrenergic blocking agents and calcium antagonists suppressed the calpain activity and decreased cell death during hypoxia. On the other hand, alpha-adrenergic blocking agents did not affect calpain activity and cell death under hypoxic conditions. These results prove that beta-adrenergic blocking agents and calcium antagonists prevent protein degradation during hypoxic cell injury.
Iizuka
K
K
Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Kawaguchi
H
H
Yasuda
H
H
D000595:Amino Acid Sequence; D000818:Animals; D002154:Calpain / Q000037:antagonists & inhibitors / Q000378:metabolism*; D016923:Cell Death; D015687:Cell Hypoxia / Q000502:physiology*; D002470:Cell Survival; D002478:Cells, Cultured; D010450:Endopeptidases / Q000378:metabolism; D007700:Kinetics; D008969:Molecular Sequence Data; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D009842:Oligopeptides / Q000138:chemical synthesis / Q000494:pharmacology*; D051381:Rats
D009842:Oligopeptides; D010450:Endopeptidases; D002154:Calpain