Signal transduction in ischemic preconditioning.
When the heart is subjected to a transient non-lethal period of ischemia, it quickly adapts itself to become resistant to infarction from a subsequent ischemic insult. This adaptation, termed preconditioning, occurs in all species studied, including man. The protection has been shown to be mediated by stimulation of adenosine and probably bradykinin receptors. Recent studies reveal that these receptors may protect by activating protein kinase C in cardiomyocytes. In this review the evidence supporting the protein kinase C hypothesis and therapeutic possibilities for employing the preconditioning phenomenon in clinical situations are discussed.
Downey
J M
JM
Department of Physiology, University of South Alabama College of Medicine, Mobile 36688, USA.
Cohen
M V
MV
D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D010739:Phospholipase D / Q000502:physiology; D011493:Protein Kinase C / Q000502:physiology; D011817:Rabbits; D018002:Receptors, Bradykinin / Q000502:physiology; D018047:Receptors, Purinergic P1 / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D018002:Receptors, Bradykinin; D018047:Receptors, Purinergic P1; D011493:Protein Kinase C; D010739:Phospholipase D