title: Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland.
abstract: OBJECTIVE
  To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide-exposed rat parotid gland.
  
  
  METHODS
  Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration.
  
  
  RESULTS
  The myeloperoxidase activity of the lipopolysaccharide-exposed gland was 10-fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin-8 (10 or 25 μg kg(-1) , given twice intraperitoneally) or melatonin (10 or 25 mg kg(-1) x 2) the lipopolysaccharide-induced response was elevated 4.6- and 3.5-folds at the most. The cholecystokinin-A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin-8, while the melatonin 2-preferring receptor antagonist luzindole had no effect on the melatonin-induced inhibition. Unselective nitric oxide-synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide-synthase (of non-nervous origin) halved the inflammatory response.
  
  
  CONCLUSIONS
  Some hormones may contribute to anti-inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide-synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.
authors.affiliation: Division of Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Göteborg, Sweden.
authors.forename: H
authors.initials: H
authors.lastname: Cevik-Aras
authors.forename: J
authors.initials: J
authors.lastname: Ekström
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D004926:Escherichia coli; D006727:Hormone Antagonists / Q000494:pharmacology; D007274:Injections, Intraperitoneal; D008070:Lipopolysaccharides / Q000009:adverse effects; D008239:Lysine / Q000031:analogs & derivatives / Q000494:pharmacology; D008550:Melatonin / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000627:therapeutic use*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D020556:Neutrophil Infiltration / Q000187:drug effects; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052248:Nitric Oxide Synthase Type I / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors; D009929:Organ Size; D017764:Parasympathectomy; D010306:Parotid Gland / Q000187:drug effects* / Q000201:enzymology / Q000294:innervation; D010309:Parotitis / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control*; D009195:Peroxidase / Q000032:analysis; D011377:Proglumide / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D043886:Receptor, Cholecystokinin A / Q000037:antagonists & inhibitors; D044123:Receptor, Melatonin, MT2 / Q000037:antagonists & inhibitors; D012844:Sincalide / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000627:therapeutic use*; D013562:Sympathectomy; D014363:Tryptamines / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D006727:Hormone Antagonists; D008070:Lipopolysaccharides; C090663:N(6)-(1-iminoethyl)lysine; D043886:Receptor, Cholecystokinin A; D044123:Receptor, Melatonin, MT2; D014363:Tryptamines; C057154:luzindole; D009195:Peroxidase; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D011377:Proglumide; D008550:Melatonin; D008239:Lysine; C048181:lorglumide; D012844:Sincalide; D019331:NG-Nitroarginine Methyl Ester