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746.17 |
Emergency Medicine, University of Iowa, 3115 Medical Laboratories, Iowa City, IA, 52242
ABSTRACT
Ischemia-reperfusion injury contributes to the pathophysiology of numerous diseases. Ischemic preconditioning increases tissue resistance to ischemia-reperfusion injury. Among the mediators of ischemic preconditioning are opioid peptides called enkephalins. We found that numerous non-neuronal tissues express the enkephalin precursor protein proenkephalin. Additionally, using isolated heart, intestine, and skeletal muscle, we found a tissue-specific pattern of enkephalin release. We also found that ischemia increased cardiac enkephalin release, and that exercise altered the efficiency of enkephalin processing and release. In addition to acting as potential sources for enkephalin release, heart, intestine, and skeletal muscle all express mRNAs for opioid receptors, suggesting that these tissues are also targets for opioid-mediated effects. Consistent with this conclusion, purified enkephalins induced opioid-dependent decreases in intestinal contractility. Taken together, our data suggest that skeletal muscle, heart, and intestine may release enkephalins that may in turn mediate autocrine, paracrine, and systemic effects, including ischemic preconditioning.
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