@entity286 -associated XXXX in smokers: role of the ET-1 pathway.

@entity1 @entity286 @entity455 @entity11345 @entity409 @entity120 @entity1617 @entity358 @entity2613 @entity11344
@entity455 associated to @entity286 smoking might pave the way for the subsequent development of @entity120 . Its prognosis is dreadful and its underlying mechanisms are so far largely unknown in @entity1 . To assess the potential role of endothelin-1 and its receptors in smokers' pulmonary artery vasoactive properties. Endothelium-dependent vasodilation to @entity1617 was assessed in @entity358 from 34 smokers and compared with that of 10 nonsmokers. The effects of ET-A ( @entity11344 ) or ET-B ( @entity11345 ) blockers and that of an ET-B activator (sarafotoxin) were evaluated. Endothelin-1 was quantitated by ELISA. Expression of its receptors was quantitated by Western blotting. Smokers exhibited an impaired pulmonary endothelium-dependent vasodilation compared with nonsmokers (P < 0.01). In the former group, 8 of 34 subjects exhibited a marked @entity409 ( @entity2613 (+)) whereas 26 ( @entity2613 (-)) (P < 10(-4)) displayed a vasorelaxation to @entity1617 that was comparable to that of nonsmokers. In @entity2613 (+) subjects, ET-A was overexpressed (P < 0.05) and inversely correlated (P < 10(-2)) with the response to @entity1617 . Sarafotoxin significantly improved vasodilation in all subjects (P < 10(-2)). In conclusion, @entity286 smoking is associated to an @entity358 at least partly mediated by an ET-1/ET-A-dependent dysfunction.
