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Article: NO and EDHF pathways in pulmonary arteries and veins are impaired in COPD patients

TitleNO and EDHF pathways in pulmonary arteries and veins are impaired in COPD patients
Authors
Issue Date2012
Citation
Vascular Pharmacology, 2012, v. 57 n. 2-4, p. 113-118 How to Cite?
AbstractWe investigated endothelial function of both pulmonary arteries and veins in patients with chronic obstructive pulmonary disease (COPD) of varying severity in regard to the role of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Lung tissues were obtained from patients undergoing lobectomy or pneumonectomy. Patients were grouped to control, moderate COPD, and severe COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Pulmonary arteries and veins were studied for endothelium-dependent relaxations. NO concentration was measured by electrochemical method. Protein expressions of eNOS and phosphorylated eNOS were determined by Western-blot. Endothelium-dependent relaxation was more significant in pulmonary arteries than in veins. The vasorelaxation was decreased in patients of moderate COPD and further decreased in severe COPD. The severity of endothelial dysfunction in both pulmonary arteries and veins correlated with the degree of airflow obstruction. COPD patients exhibited reduced endothelial NO production, decreased eNOS protein expression and decreased eNOS phosphorylation. The EDHF component was abolished in the pulmonary vasculature of patients with severe COPD. NO and EDHF pathways are both involved in the regulation of vascular tone in human pulmonary arteries and veins. Both pathways are impaired in COPD patients and the severity of the impairment increases with the progress of the disease. Downregulation of eNOS expression and inhibition of eNOS activation underlie the reduction of NO in COPD patients. © 2012 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/192690
ISSN
2015 Impact Factor: 2.5
2015 SCImago Journal Rankings: 1.204
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYang, Qen_US
dc.contributor.authorShigemura, Nen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorHsin, Men_US
dc.contributor.authorXue, H-Men_US
dc.contributor.authorHuang, Yen_US
dc.contributor.authorHe, G-Wen_US
dc.contributor.authorYu, C-Men_US
dc.date.accessioned2013-11-20T04:55:22Z-
dc.date.available2013-11-20T04:55:22Z-
dc.date.issued2012en_US
dc.identifier.citationVascular Pharmacology, 2012, v. 57 n. 2-4, p. 113-118en_US
dc.identifier.issn1537-1891en_US
dc.identifier.urihttp://hdl.handle.net/10722/192690-
dc.description.abstractWe investigated endothelial function of both pulmonary arteries and veins in patients with chronic obstructive pulmonary disease (COPD) of varying severity in regard to the role of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Lung tissues were obtained from patients undergoing lobectomy or pneumonectomy. Patients were grouped to control, moderate COPD, and severe COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Pulmonary arteries and veins were studied for endothelium-dependent relaxations. NO concentration was measured by electrochemical method. Protein expressions of eNOS and phosphorylated eNOS were determined by Western-blot. Endothelium-dependent relaxation was more significant in pulmonary arteries than in veins. The vasorelaxation was decreased in patients of moderate COPD and further decreased in severe COPD. The severity of endothelial dysfunction in both pulmonary arteries and veins correlated with the degree of airflow obstruction. COPD patients exhibited reduced endothelial NO production, decreased eNOS protein expression and decreased eNOS phosphorylation. The EDHF component was abolished in the pulmonary vasculature of patients with severe COPD. NO and EDHF pathways are both involved in the regulation of vascular tone in human pulmonary arteries and veins. Both pathways are impaired in COPD patients and the severity of the impairment increases with the progress of the disease. Downregulation of eNOS expression and inhibition of eNOS activation underlie the reduction of NO in COPD patients. © 2012 Elsevier Inc.en_US
dc.languageengen_US
dc.relation.ispartofVascular Pharmacologyen_US
dc.titleNO and EDHF pathways in pulmonary arteries and veins are impaired in COPD patientsen_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.vph.2012.05.004en_US
dc.identifier.pmid22609132-
dc.identifier.scopuseid_2-s2.0-84865405670en_US
dc.identifier.volume57en_US
dc.identifier.issue2-4en_US
dc.identifier.spage113en_US
dc.identifier.epage118en_US
dc.identifier.isiWOS:000308388600009-

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