dc.creator | Kitsiopoulou, E. | en |
dc.creator | Hatziefthimiou, A. A. | en |
dc.creator | Gourgoulianis, K. I. | en |
dc.creator | Molyvdas, P. A. | en |
dc.date.accessioned | 2015-11-23T10:34:55Z | |
dc.date.available | 2015-11-23T10:34:55Z | |
dc.date.issued | 2007 | |
dc.identifier | 10.1155/2007/24174 | |
dc.identifier.issn | 0962-9351 | |
dc.identifier.uri | http://hdl.handle.net/11615/29439 | |
dc.description.abstract | The alteration of resting tension (RT) from 0.5 g to 2.5 g increased significantly airway smooth muscle contractions induced by acetylcholine (ACh) in rabbit trachea. The decrease in extracellular calcium concentration [Ca(2+)](o) from 2mM to 0.2mM reduced ACh-induced contractions only at 2.5 g RT with no effect at 0.5 g RT. The nonselective inhibitor of nitric oxide synthase (NOS), N(G)-nitro-L-arginine methyl ester (L-NAME) increased ACh-induced contractions at 2.5 g RT. The inhibitor of inducible NOS, S-methylsothiourea or neuronal NOS, 7-nitroindazole had no effect. At 2.5 g RT, the reduction of [Ca2+] o from 2mM to 0.2mM abolished the e. ect of L-NAME on ACh-induced contractions. The NO precursor L-arginine or the tyrosine kinase inhibitors erbstatin A and genistein had no effect on ACh-induced contractions obtained at 2.5 g RT. Our results suggest that in airways, RT affects ACh-induced contractions by modulating the activity of epithelial NOS in a calcium-dependent, tyrosine- phosphorylation-independent way. | en |
dc.source | Mediators of Inflammation | en |
dc.source.uri | <Go to ISI>://WOS:000248216300001 | |
dc.subject | NITRIC-OXIDE SYNTHASE | en |
dc.subject | SMOOTH-MUSCLE-CELLS | en |
dc.subject | DEEP INSPIRATION | en |
dc.subject | EPITHELIAL-CELLS | en |
dc.subject | CA2+-INDEPENDENT ACTIVATION | en |
dc.subject | ISOMETRIC CONTRACTION | en |
dc.subject | PULMONARY-ARTERIES | en |
dc.subject | CA2+ CONCENTRATION | en |
dc.subject | CYCLIC-AMP | en |
dc.subject | L-ARGININE | en |
dc.subject | Cell Biology | en |
dc.subject | Immunology | en |
dc.title | Resting tension affects eNOS activity in a calcium- dependent way in airways | en |
dc.type | journalArticle | en |