Rationale: Cardiovascular disease is a major cause of morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), which may in part be attributable to abnormalities of systemic vascular function. It is unclear whether such associations relate to the presence of COPD or prior smoking habit. Objectives: To undertake a comprehensive assessment of vascular function in patients with COPD and healthy controls matched for smoking history. Methods: Eighteen men with COPD were compared with 17 healthy male controls matched for age and lifetime cigarette smoke exposure. Participants were free from clinically evident cardiovascular disease. Measurements and main results: Pulse wave velocity (PWV) and pulse wave analysis were measured via applanation tonometry at carotid, radial and femoral arteries. Blood flow was measured in both forearms using venous occlusion plethysmography during intra-brachial infusion of endothelium-dependent vasodilators (bradykinin, 100-1000 pmol/min; acetylcholine, 5-20 µg/min) and endothelium-independent vasodilators (sodium nitroprusside, 2-8 µg/min; verapamil, 10-100 µg/min). Tissue plasminogen activator (t-PA) was measured in venous plasma before and during bradykinin infusions. Patients with COPD have greater arterial stiffness (PWV, 11±2 vs 9±2 m/s; p=0.003: augmentation index, 27±10 vs 21±6 %, p=0.028), but there were no differences in endothelium-dependent and –independent vasomotor function or bradykinin-induced endothelial t-PA release (p>0.05 for all). Conclusions: COPD is associated with increased arterial stiffness independent of cigarette smoke exposure. However, this abnormality is not explained by systemic endothelial dysfunction. Increased arterial stiffness may represent the mechanistic link between COPD and the increased risk of cardiovascular disease associated with this condition.