COPD (chronic obstructive pulmonary disease) is a significant health concern as the fourth leading cause of morbidity and mortality in the U.S.A. Although the prevalence of PH (pulmonary hypertension) in COPD is unknown, its presence is a risk factor for mortality. In this comment, we consider the role of PH in COPD and its pathophysiology, with reference to ET-1 (endothelin-1) and cigarette smoke, as well as exercise and nocturnal hypoxia. We also explore potential mechanisms for the observed improvement in exercise tolerance following 6 months of pravastatin treatment in COPD patients with PH as reported by Lee and co-workers in the present issue of Clinical Science, including possible effects upon ET-1 and Rho kinase, or antioxidant effects, which may be particularly relevant in this group of mainly current smokers.