2019
DOI: 10.1186/s12931-019-1133-8
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Dysregulation of the endothelial nitric oxide pathway is associated with airway inflammation in COPD

Abstract: Background Chronic obstructive pulmonary disease (COPD) is related to endothelial dysfunction and the impaired generation of nitric oxide (NO) from L-arginine by the endothelial NO synthase (eNOS). The relationship between eNOS dysfunctionality and airway inflammation is unknown. We assessed serum asymmetric and symmetric dimethylarginine (ADMA and SDMA) and nitrite/nitrate concentrations, indicators of eNOS function, in patients with COPD and correlated them with markers of inflammation. … Show more

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Cited by 43 publications
(31 citation statements)
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References 46 publications
(51 reference statements)
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“…The vulnerable populations in the current pandemic may have lower levels of endogenously produced NO. NO generated from eNOS drops off with age, and patients with chronic vascular inflammation, such as in type 2 diabetes, metabolic syndrome, chronic obstructive pulmonary disease, obesity, autoimmune disorders and hemoglobinopathies, may produce less eNOS [ 34 , 39 , 40 ]. Additionally, ACE activity relative to ACE2 activity may be elevated in patients with chronic vascular inflammation [ 41 , 42 ].…”
Section: The Rationale For Nitric Oxide Usementioning
confidence: 99%
“…The vulnerable populations in the current pandemic may have lower levels of endogenously produced NO. NO generated from eNOS drops off with age, and patients with chronic vascular inflammation, such as in type 2 diabetes, metabolic syndrome, chronic obstructive pulmonary disease, obesity, autoimmune disorders and hemoglobinopathies, may produce less eNOS [ 34 , 39 , 40 ]. Additionally, ACE activity relative to ACE2 activity may be elevated in patients with chronic vascular inflammation [ 41 , 42 ].…”
Section: The Rationale For Nitric Oxide Usementioning
confidence: 99%
“…The reasons why COPD patients with PVD show greater systemic vascular disease are not clear. Airway inflammation has been previously linked with reduced vascular nitric oxide production, 27 which could possibly explain a mechanism for endothelial dysfunction. However, the hypothesis of a "spillover" of inflammatory mediators from the lung to the systemic circulation is not supported by the current findings, since there were no consistent differences among groups in the inflammatory mediators that were tested.…”
Section: Discussionmentioning
confidence: 99%
“…These molecules play important role in the leukocyte adhesion and in the rolling to the focus of the inflammatory process although others factors are important to the leukocyte migration phenomenon. NO is an important mediator in the leukocyte migration, promoting vasodilation and reducing the recruitment, adhesion, rolling, and leukocyte migration during inflammatory response favoring diapedesis [ 40 , 41 ]. Since EEGC did not increase the NO levels induced by zymosan, it led us to conclude that the EEGC mechanism of action was not involved in the NO pathway.…”
Section: Discussionmentioning
confidence: 99%