Reduced expression of endothelial nitric oxide synthase in pulmonary arteries of smokers

Citation
Ja. Barbera et al., Reduced expression of endothelial nitric oxide synthase in pulmonary arteries of smokers, AM J R CRIT, 164(4), 2001, pp. 709-713
Citations number
37
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
164
Issue
4
Year of publication
2001
Pages
709 - 713
Database
ISI
SICI code
1073-449X(20010815)164:4<709:REOENO>2.0.ZU;2-R
Abstract
Cigarette smoking has been associated with alterations in the structure and endothelial function of pulmonary arteries. Nitric oxide (NO) and endothel in-1 are endothelium-derived mediators with opposite effects on vascular to ne and cell growth. To investigate whether cigarette smoking could induce c hanges in the synthesis of these mediators in pulmonary arteries, we compar ed the expression of both endothelial NO synthase (eNOS) and endothelin-1 i n the lungs of smokers with that in nonsmokers. Lung tissue samples of 23 s mokers and nine nonsmokers were studied. Expression of eNOS and endothelin- 1 in pulmonary artery endothelium was evaluated by immunohistochemistry. In protein extracts of lung tissue, the content of eNOS protein was assessed by Western blot analysis and that of endothelin-1 by radioimmunoassay. The immunohistochemical expression of eNOS in arterial endothelium and the eNOS protein content in lung tissue were lower in the smokers than in the nonsm okers. No differences were shown in cell expression and protein content of endothelin-1 between both groups. We conclude that cigarette smoking is ass ociated with reduced expression of eNOS in pulmonary arteries. The diminish ed synthesis of nitric oxide may contribute to the alterations in the struc ture and endothelial function of pulmonary vessels in cigarette-smoke-induc ed respiratory disease.