Acute and chronic cardioprotection by the enkephalin analogue, Eribis peptide 94, is mediated via activation of nitric oxide synthase and adenosine triphosphate-regulated potassium channels. Pharmacology 2012;90(1-2):110-6
Date
07/21/2012Pubmed ID
22814415Pubmed Central ID
PMC3482344DOI
10.1159/000340058Scopus ID
2-s2.0-84863873307 (requires institutional sign-in at Scopus site) 11 CitationsAbstract
BACKGROUND/AIMS: Eribis peptide 94 (EP 94) is a new enkephalin derivative which potently binds to the µ- and δ-opioid receptor. In this study, we determined the effects of EP 94 and potential mechanism(s) involved in cardioprotection of the rat heart.
METHODS AND RESULTS: An acute (5 and10 min into ischemia) and a chronic (24 h prior to ischemia) EP 94 administration produced a similar 30-40% reduction in infarct size/area at risk and the effects were blocked by the K(ATP) channel antagonists, HMR 1098 and 5-HD. The cardioprotective effects were blocked by a nonselective nitric oxide synthase (NOS) inhibitor (L-NAME) following acute administration and by a selective iNOS inhibitor (1400W) following chronic administration.
CONCLUSION: These results suggest that EP 94 may have potential for the treatment of ischemic heart disease via a nitric oxide (NO)-K(ATP)-mediated mechanism.
Author List
Gross GJ, Hsu A, Nithipatikom K, Pfeiffer AW, Bobrova I, Bissessar EMESH terms used to index this publication - Major topics in bold
AnimalsBenzamides
Cardiotonic Agents
Decanoic Acids
Enkephalins
Hydroxy Acids
KATP Channels
Male
Myocardial Reperfusion Injury
Nitric Oxide
Nitric Oxide Synthase
Nitric Oxide Synthase Type II
Potassium Channel Blockers
Rats
Rats, Sprague-Dawley
Receptors, Opioid, delta
Receptors, Opioid, mu
