The GPCR OGR1 (GPR68) mediates diverse signalling and contraction of airway smooth muscle in response to small reductions in extracellular pH

BACKGROUND AND PURPOSE Previous studies have linked a reduction in pH in airway, caused by either environmental factors, microaspiration of gastric acid or inflammation, with airway smooth muscle (ASM) contraction and increased airway resistance. Neural mechanisms have been shown to mediate airway c...

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Veröffentlicht in:	British journal of pharmacology 2012-06, Vol.166 (3), p.981-990
Hauptverfasser:	Saxena, H, Deshpande, DA, Tiegs, BC, Yan, H, Battafarano, RJ, Burrows, WM, Damera, G, Panettieri, RA, DuBose Jr, TD, An, SS, Penn, RB
Format:	Artikel
Sprache:	eng
Schlagworte:	airway smooth muscle asthma Biological and medical sciences Bronchi - cytology Bronchi - drug effects bronchoconstriction calcium cAMP‐dependent protein kinase Cell Culture Techniques Cells, Cultured Chronic obstructive pulmonary disease, asthma contraction Cyclic AMP - metabolism Cyclooxygenase Inhibitors - pharmacology Dose-Response Relationship, Drug Extracellular Fluid - chemistry G protein‐coupled receptor GPR68 Humans Hydrochloric Acid - pharmacology Hydrogen-Ion Concentration Indomethacin - pharmacology inflammation Medical sciences Muscle Contraction - drug effects Muscle, Smooth - cytology Muscle, Smooth - drug effects Muscle, Smooth - metabolism Muscular system OGR1 Pharmacology. Drug treatments Pneumology Real-Time Polymerase Chain Reaction Receptors, G-Protein-Coupled - metabolism Receptors, G-Protein-Coupled - physiology Research Papers Signal Transduction - drug effects Signal Transduction - physiology Smooth muscle Trachea - cytology Trachea - drug effects
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Beschreibung
Zusammenfassung:	BACKGROUND AND PURPOSE Previous studies have linked a reduction in pH in airway, caused by either environmental factors, microaspiration of gastric acid or inflammation, with airway smooth muscle (ASM) contraction and increased airway resistance. Neural mechanisms have been shown to mediate airway contraction in response to reductions in airway pH to
ISSN:	0007-1188 1476-5381
DOI:	10.1111/j.1476-5381.2011.01807.x