Abstract
Background: Pulmonary hypertension secondary to COPD is characterized principally by impairment of vasoreactivity and vascular remodeling. While the structural changes have been described in all stages of COPD, the impairment of vasoreactivity in response to ET-1, a potent vasoconstrictor, has not been well understood. Materials and methods: Proximal pulmonary arteries were obtained from non-smokers, smokers with normal lung function, and COPD patients who underwent lung resection for other diseases (n=6 in each group). Pulmonary arterial contraction induced by ET-1 was assessed without or with the presence of ET-1 receptor antagonists (BQ- 123 and BQ-788). Expressions of ET-1 receptors were measured by immunohistochemistry, western blot, and qRTPCR. Results: ET-1-induced pulmonary arterial contraction increased significantly in COPD patients in comparison with control subjects and non-COPD smokers (P<0.05) and the use of ET-1 receptor antagonists could not prevent this contraction. The hypercontraction was not associated with the increase of ET-1 and ET-1 receptors expression in pulmonary arterial vessels. Conclusion: In patients with COPD, pulmonary arterial contraction induced by ET-1 has increased significantly and could not be prevented by using ET-1 receptor antagonist alone. This alteration might be related to the upreguation of other signalling pathways in pulmonary arterial vessels of COPD patients.
Highlights
In patients with chronic obstructive pulmonary disease (COPD), the impairment of vasoreactivity in response to endothelium-derived constricting factor and relaxing factors has not been well understood
In patients with COPD, pulmonary arterial contraction induced by ET-1 has increased significantly and could not be prevented by using ET-1 receptor antagonist alone
This alteration might be related to the upreguation of other signalling pathways in pulmonary arterial vessels of COPD patients
Summary
In patients with chronic obstructive pulmonary disease (COPD), the impairment of vasoreactivity in response to endothelium-derived constricting factor (endothelin-1, thromboxane) and relaxing factors (nitric oxide, prostacyclin) has not been well understood. This impairment might be due to endothelial dysfunction and might promote to the alteration of pulmonary vascular tone and pulmonary vascular hypertrophy in these patients [1]. The effect of cigarette smoke on systemic vascular tone due to ET-1 by increasing the vasoconstriction has been well studied [4], the vasoreactivity of pulmonary vessels in response to ET-1 in healthy smokers and especially in smokers with COPD has not been well understood. While the structural changes have been described in all stages of COPD, the impairment of vasoreactivity in response to ET-1, a potent vasoconstrictor, has not been well understood
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