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Role of PGE 2 /EP 2 Receptor Signaling on The Effects of Neonatal Hyperoxia on Airway Smooth Muscle
Author(s) -
Sopi Ramadan,
Mladenov Mitko,
Dreshaj Ismail,
Neziri Burim,
Mehmeti Mirsad,
Bislimi Kemajl,
Jakupaj Muharrem
Publication year - 2015
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.29.1_supplement.1030.7
Subject(s) - hyperoxia , agonist , prostaglandin f2alpha , antagonist , endocrinology , prostaglandin e , medicine , chemistry , muscle relaxation , receptor , prostaglandin , anesthesia , pharmacology , lung
It was shown that neonatal hyperoxic‐exposure associates with airway hyperresponsiveness and impaired nonadrenergic noncholinergic relaxation. It was demonstrated that reduced relaxant responses were associated with an impairment of prostaglandin E 2 (PGE 2 ) release from airway smooth muscle (ASM). In this study we tested the hypothesis that supplementation of PGE 2 or EP 2 agonists to ASM restore relaxant responses. Tracheal cylinders were obtained from 12 days rat pups exposed to hyperoxia or room air for seven days. These cylinders were used to study contractile and relaxant responses. In hyperoxic tracheal preparations the contractile responses to bethanechol were enhanced as compared to room air controls. These enhanced contractile responses were attenuated by pre‐incubation of tissues with PGE 2 (1µM). Similar effect was showed by using an EP 2 agonist. This effect of PGE 2 and EP 2 agonist was reversed by an EP 2 antagonist. PGE 2 and EP 2 induced dose response relaxations of ASM, which were reduced by an EP 2 antagonist. We conclude that PGE 2 induces relaxation of airways via EP 2 receptors, and the use of EP 2 agonists may serve as a therapeutic approach to overcome the adverse effects of neonatal hyperoxia on relaxant responses of ASM. Support by MEST