Delta-opioid receptor-induced late preconditioning is mediated by cyclooxygenase-2 in conscious rabbits

Am J Physiol Heart Circ Physiol. 2002 Nov;283(5):H1943-57. doi: 10.1152/ajpheart.00150.2002.

Abstract

Although activation of delta-opioid receptors is known to induce both early and late preconditioning (PC) against myocardial infarction, the mechanisms for this salubrious effect are unclear. Furthermore, it is unknown whether delta-opioid receptors can also induce late PC against myocardial stunning. By using conscious rabbits (n = 120) in this study, we found that the delta-opioid receptor agonist (+/-)-4-[(alpha-R*)-alpha-[(2S*,5R*)-4-allyl-2,5-dimethyl-1-piperazinyl]-3-hydroxybenzyl]-N,N-diethylbenzamide (BW-373U86) induced late PC against myocardial stunning 24 h after treatment and that this effect was abolished by the selective cyclooxygenase-2 (COX-2) inhibitors N-[2-(cyclohexyloxy)4-nitrophenyl]methanesulfonamide (NS-398) and celecoxib. This protective effect was also abrogated by the selective delta(1)-opioid receptor antagonist 7-benzylidenenaltrexone, indicating that the delta(1)-opioid receptor is necessary for BW-373U86-induced late PC. BW-373U86 did not induce early PC against stunning. In addition, BW-373U86 induced late PC against infarction, which was blocked by NS-398. At 24 h after BW-373U86 administration, myocardial COX-2 protein expression and PGE(2) and 6-keto-PGF(1alpha) levels were significantly increased. These results demonstrate that activation of delta-opioid receptors induces late PC against both stunning and infarction via a COX-2-dependent mechanism.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / analysis
  • Animals
  • Benzamides / pharmacology
  • Benzylidene Compounds / pharmacology
  • Celecoxib
  • Consciousness
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / pharmacology
  • Dinoprostone / analysis
  • Heart Rate / drug effects
  • Ischemic Preconditioning, Myocardial*
  • Isoenzymes / antagonists & inhibitors
  • Isoenzymes / metabolism*
  • Male
  • Myocardial Infarction / drug therapy
  • Myocardial Infarction / metabolism
  • Myocardial Stunning / drug therapy
  • Myocardial Stunning / metabolism*
  • Myocardium / chemistry
  • Myocardium / enzymology
  • Naltrexone / analogs & derivatives*
  • Naltrexone / pharmacology
  • Narcotic Antagonists / pharmacology
  • Nitrobenzenes / pharmacology
  • Piperazines / pharmacology
  • Prostaglandin-Endoperoxide Synthases / metabolism*
  • Pyrazoles
  • Rabbits
  • Receptors, Opioid, delta / metabolism*
  • Sulfonamides / pharmacology

Substances

  • Benzamides
  • Benzylidene Compounds
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Isoenzymes
  • Narcotic Antagonists
  • Nitrobenzenes
  • Piperazines
  • Pyrazoles
  • Receptors, Opioid, delta
  • Sulfonamides
  • N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
  • 7-benzylidenenaltrexone
  • BW 373U86
  • 6-Ketoprostaglandin F1 alpha
  • Naltrexone
  • Cyclooxygenase 2
  • Prostaglandin-Endoperoxide Synthases
  • Celecoxib
  • Dinoprostone