Role of Endogenous Agonists of Opioid Receptors in the Regulation of Heart Resistance to Postischemic Reperfusion Injury

Bull Exp Biol Med. 2017 Nov;164(1):18-20. doi: 10.1007/s10517-017-3916-6. Epub 2017 Nov 9.

Abstract

Intravenous injection of nonselective antagonists of opioid receptors (OR) naltrexone (5 mg/kg) and naloxone methiodide (5 mg/kg), selective δ1-OR antagonist BNTX (0.7 mg/kg), selective δ2-OR blocker naltriben (0.3 mg/kg), selective κ-OR antagonist norbinaltorphimine (2 mg/kg), and selective blocker of ORL1 opioid receptors JTC-801 (0.1 mg/kg) produced no effect on reperfusion injury to the heart in rats narcotized with α-chloralose. In contrast, selective μ-OR antagonist CTAP (1 mg/kg) limited the infarct size, although this effect was not observed at a lower CTAP concentration of 0.1 mg/kg. Probably, the myocardial infarct size-limiting effect of CTAP was associated with activation of the non-opioid receptors. It was hypothesized that endogenous OR agonists did not affect heart resistance to reperfusion injury in unadapted rats.

Keywords: heart; opioid receptors; opioids; rat; reperfusion.

MeSH terms

  • Analgesics, Opioid / pharmacology
  • Animals
  • Cardiotonic Agents / pharmacology
  • Disease Resistance
  • Heart Rate
  • Male
  • Myocardial Reperfusion Injury / metabolism*
  • Myocardium / pathology
  • Narcotic Antagonists / pharmacology
  • Peptide Fragments / pharmacology
  • Peptide Fragments / physiology
  • Protective Factors
  • Rats, Wistar
  • Receptors, Opioid / physiology*
  • Somatostatin / pharmacology
  • Somatostatin / physiology

Substances

  • Analgesics, Opioid
  • CTAP octapeptide
  • Cardiotonic Agents
  • Narcotic Antagonists
  • Peptide Fragments
  • Receptors, Opioid
  • Somatostatin