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PROSTAGLANDINS, CAPSAICIN‐SENSITIVE SENSORY NERVES AND NEUTROPHIL INFILTRATION, BUT NOT NITRIC OXIDE, CONTRIBUTE TO COLD RESTRAINT STRESS‐INDUCED GASTRIC ADAPTATION IN RATS
Author(s) -
Tan Ruken,
Bülbül Mehmet,
Öngüt Gözde,
Tosun Özgür,
İzgütUysal V Nimet
Publication year - 2006
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2006.04469.x
Subject(s) - capsaicin , nitric oxide , calcitonin gene related peptide , stomach , endocrinology , medicine , infiltration (hvac) , chemistry , sensory nerve , receptor , sensory system , neuropeptide , biology , physics , neuroscience , thermodynamics
SUMMARY1 The aim of the present study was to determine the role of prostaglandins (PG), nitric oxide (NO) and capsaicin‐sensitive sensory nerves in neutrophil infiltration in gastric adaptation to cold restraint stress in rats. 2 Wistar rats were exposed to single or repeated cold restraint stress for 3.5 h every other day for up to 4 days. Prior to repeated stress, rats were pretreated with N G ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME; 10 mg/kg, s.c.), indomethacin (10 mg/kg, s.c.) or capsaicin (125 mg/kg, s.c.). The extent of gastric mucosal lesions was evaluated histologically and myeloproxidase (MPO) activity, PGE 2 , NO and calcitonin gene‐related peptide (CGRP) levels were measured in gastric tissue. 3 Cold restraint stress produced haemorrhagic lesions and reduced PGE 2 and CGRP levels in the stomach, with an increase in MPO activity and NO levels. Repeated stress insults reduced stress‐induced gastric damage, NO production and MPO activity, with an increase in PGE 2 and CGRP levels compared with rats exposed to single cold restraint stress. Adaptation to cold restraint stress was prevented by indomethacin and capsaicin pretreatment, but not by l ‐NAME. 4 We conclude that the stomach has the ability to adapt to repeated exposure to cold restraint stress and that the adaptation, via inhibition of neutrophil infiltration, is mediated, at least in part, by endogenous PG and CGRP.