title: Relation of adrenergic receptors, which have roles in gastroprotective and anti-inflammatory effect of adrenal gland hormones, with cyclooxygenase enzyme levels in rats.
abstract: OBJECTIVE
  COX-2 enzyme inhibition is responsible for the anti-inflammatory effects of NSAIDs, COX-1 for their effects upon the gastrointestinal system (GIS), along with other side effects. We investigated the relationship between COX levels and those adrenergic receptors known to play a role in gastroprotection and anti-inflammatory activity.
  
  
  METHODS
  The effects of adrenaline and prednisolone on gastric COX-1 and COX-2 levels in both intact and adrenalectomized rats treated with doxazosin, yohimbine, propranolol, and metoprolol were determined.
  
  
  RESULTS
  We found that adrenaline increases COX-1 levels in the gastric tissue of both intact and adrenalectomized rats by stimulating alpha-2 receptors. Adrenaline decreases COX-2 levels by stimulating beta-2 adrenergic receptors. Prednisolone inhibits both COX-1 and COX-2 in the gastric tissue of intact rats. In adrenalectomized rats, prednisolone increases gastric COX-1 by stimulating alpha-2 receptors, and decreases COX-2 levels by stimulating beta-2 receptors.
  
  
  CONCLUSIONS
  Prednisolone cannot bind to a adrenergic receptors in the presence of adrenaline (intact rats) but, in its absence (adrenalectomy), binds to alpha-2 receptors, and stimulates them more effectively than adrenaline, suggesting a direct relationship between alpha-2 adrenergic receptors and COX-1 levels, whereas beta-2 receptors are directly related to COX-2 levels.
authors.affiliation: Faculty of Medicine, Department of Pharmacology, Ataturk University, Erzurum, Turkey. halis.suleyman@gmail.com
authors.forename: H
authors.initials: H
authors.lastname: Suleyman
authors.forename: H
authors.initials: H
authors.lastname: Dursun
authors.forename: M
authors.initials: M
authors.lastname: Bilici
authors.forename: E
authors.initials: E
authors.lastname: Cadirci
authors.forename: Z
authors.initials: Z
authors.lastname: Halici
authors.forename: M
authors.initials: M
authors.lastname: Gulaboglu
authors.forename: F
authors.initials: F
authors.lastname: Albayrak
mesh_terms: D000315:Adrenalectomy; D018674:Adrenergic Antagonists / Q000494:pharmacology; D058647:Adrenergic alpha-2 Receptor Agonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D058666:Adrenergic beta-2 Receptor Agonists; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D051545:Cyclooxygenase 1 / Q000378:metabolism*; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D004837:Epinephrine / Q000494:pharmacology*; D008297:Male; D011239:Prednisolone / Q000494:pharmacology*; D020033:Protein Isoforms / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D011941:Receptors, Adrenergic / Q000378:metabolism*; D013270:Stomach / Q000187:drug effects / Q000201:enzymology
chemical_list: D018674:Adrenergic Antagonists; D058647:Adrenergic alpha-2 Receptor Agonists; D000316:Adrenergic alpha-Agonists; D058666:Adrenergic beta-2 Receptor Agonists; D000318:Adrenergic beta-Agonists; D020033:Protein Isoforms; D011941:Receptors, Adrenergic; D011239:Prednisolone; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D004837:Epinephrine