Objective: To investigate the roles of urotensin II (U-II) in chronic obstructive pulmonary disease (COPD).
Methods: Plasma and induced sputum were obtained from thirty four patients with stable COPD and ten healthy volunteers. The levels of U-II in plasma and induced sputum were measured by RIA kit. Lung function was performed routinely. Induced sputum cells were counted with hemacytometer and differentiated with Wright-Giemsa stain.
Results: The levels of U-II in induced sputum were 82 and 65 folds higher than those of plasma U-II in COPD patients and healthy controls (P<0.01). The levels of U-II in plasma were unrelated to those of induced sputum (r = 0.168, P>0.05). No difference was noted between COPD and healthy controls in the plasma U-II levels [1.46(1.15, 1.73) vs 1.61(1.31, 2.17) microg/L, medians with interquartile ranges, P>0.05]. Sputum U-II levels from COPD patients were 15% higher than those of healthy controls [119.87(105.03, 132.60) vs 104.44 (56.33, 122.24) microg/L, medians with interquartile ranges, P<0.05]. Induced sputum U-II levels of COPD patients had a trend of increase as lung function deteriorated and smoking index increases. Raised sputum total cell and neutrophil counts correlated strongly with the levels of U-II in induced sputum (r = 0.454, r = 0.431, both P<0.01). The levels of U-II in induced sputum correlated negatively with FEV(1)% predicted and p(O(2)) (r = -0.417, r = -0.518, both P<0.05).
Conclusion: U-II may act locally, or, via paracrine or autocrine way, play a role in the mechanism of the airway inflammation and airway remodeling in COPD.