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Pharmacological differences between two mechanistically similar drug effects, nitrous oxide (N 2 O)‐ and hyperbaric oxygen (HBO 2 )‐induced antinociception in mice
Author(s) -
Dupic Christine M.,
Zhang Yangmiao,
Shirachi Donald Y.,
Quock Raymond M.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.662.7
Subject(s) - pharmacology , captopril , antagonism , antagonist , chemistry , nociception , κ opioid receptor , opioid , receptor , medicine , endocrinology , biochemistry , blood pressure
N 2 O‐ and HBO 2 ‐induced antinociceptive effects both appear to involve an NO‐cyclic GMP‐protein kinase G‐dependent release of dynorphin that activates kappa opioid receptors. This study was conducted to further differentiate between their mechanisms of action. Antinociceptive responsiveness of male NIH Swiss mice to N 2 O and HBO 2 was assessed using the acetic acid‐induced abdominal constriction test. Pretreatment drugs were the CB 1 antagonist AM 251, the angiotensin‐converting enzyme (ACE)‐inhibitor captopril and the GABA antagonist SR‐25531. Control mice responded to N 2 O and HBO 2 with a robust antinociceptive effect. N 2 O‐induced antinociception was antagonized by AM 251 but was resistant to antagonism by captopril and SR‐95531. HBO 2 ‐induced antinociception was dose‐dependently antagonized by captopril but resistant to antagonism by AM 251 and SR‐95531. These results suggest that there are mechanisms that differentially modulate the antinociceptive responses to N 2 O and HBO 2 , notably involvement of ACE and CB 1 but not GABA mechanisms. (This research was supported by NIH Grant GM‐77153, the Allen I. White Distinguished Professorship and an institutional Summer Undergraduate Research Fellowship (SURF) Award from the American Society for Pharmacology and Experimental Therapeutics).