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Modulation by opioids and by afferent sensory neurones of prostanoid protection of the rat gastric mucosa
Author(s) -
Esplugues J.V.,
Whittle B.J.R.,
Moncada S.
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb14423.x
Subject(s) - prostanoid , sensory system , gastric mucosa , afferent , neuroscience , nociceptor , medicine , nociception , modulation (music) , receptor , stomach , biology , philosophy , aesthetics
1 Pretreatment with capsaicin, to deplete sensory neuropeptides from primary afferent neurones or the administration of morphine (9 mg kg −1 , i.v.), which can inhibit neuropeptide release, augmented gastric mucosal injury induced by a 5 min challenge with intragastric ethanol in the rat, as assessed by macroscopic and histological evaluation. 2 Morphine administration substantially attenuated the protective actions of the prostaglandin analogue 16,16 dimethyl prostaglandin E 2 (dm PGE 2 ; 0.5–20 μg kg −1 , p.o.) against ethanol‐induced damage. This reduced degree of protection by dmPGE 2 was not however, the consequence of the enhanced level of damage. 3 These actions of morphine in reducing prostaglandin protection against mucosal injury were abolished by pretreatment (5 min) with naloxone (1 mg kg −1 , i.v.) or the peripherally acting opioid antagonist, N‐methyl nalorphine (6 mg kg −1 , i.v.). 4 Capsaicin pretreatment (2 weeks before study), likewise attenuated the protective actions of dmPGE 2 , although to a lesser degree than did morphine. 5 These findings, thus implicate the involvement of capsaicin‐ and opioid‐sensitive afferent neurones in the processes by which exogenous prostanoids can protect the gastric mucosa from damage.