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Muscarinic receptor agonist‐induced constriction of airway smooth muscle is attenuated by carbon monoxide via increased cGMP production (1174.4)
Author(s) -
Jakupaj Muharrem,
Lajçi Azem,
Temaj Gazmend,
Cenaj Asllan,
Sopi Ramadan
Publication year - 2014
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.28.1_supplement.1174.4
Subject(s) - muscarinic acetylcholine receptor , chemistry , muscarinic agonist , agonist , bronchoconstriction , methacholine , stimulation , acetylcholine , tachyphylaxis , pharmacology , endocrinology , medicine , constriction , receptor , biochemistry , airway , anesthesia , lung , respiratory disease
Previously we have shown that carbon monoxide (CO) potentiates electrical field stimulation‐induced relaxation of airway smooth muscle (ASM). However, the effect of CO on ASM contractile responses induced by muscarinic receptor signaling is not well understood. Therefore, this study aimed to investigate the effect of CO on contractile responses of rat tracheal smooth muscle (TSM) induced by a muscarinic agonist. Tracheal segments were excised from 28 day‐old rats. Dose‐response curves to methacholine (MCh) were constructed in absence or presence of the CO precursor ‐ hematin (10 µM); heme oxigenase (HO) inhibitor tin protoporphyrin‐IX (SnPP‐IX; 100 µM); and/or soluble guanylyl cyclase inhibitor 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ; 10 µM). Preincubation of tissues with CO precursor ‐ hematin attenuated the MCh‐induced contractile responses of TSM. This effect of hematin was reversed by SnPP‐IX and/or ODQ, indicating the role of CO. According to the results we conclude that CO or its precursors might be an important target therapy to be used for treatment of medical conditions associated with airway hyper‐constriction.