Pulmonary hypertension, generally defined by a resting pulmonary artery mean pressure higher than 20 mmHg, is a common complication of advanced chronic obstructive pulmonary disease (COPD). Pulmonary hypertension in COPD is of the "precapillary type" and is almost exclusively accounted for by the increased pulmonary vascular resistance (PVR). Among the factors leading to an increased PVR, acute as well as chronic alveolar hypoxia is by far the most important. Pulmonary hypertension is usually mild (between 20 and 35 mmHg) in COPD patients, but pulmonary artery pressure (PAP) may increase markedly and suddenly during exercise, sleep and episodes of acute respiratory failure. These acute increases of afterload can favour the development of right heart failure. Furthermore, even if the progression of pulmonary hypertension is rather slow (PAP increases by + 0.5 mmHg/year as a mean), the level of PAP is a good indicator of prognosis in COPD patients. Consequently the treatment of pulmonary hypertension is justified in COPD. There are two treatments available so far, which are not mutually exclusive: vasodilators and long-term oxygen therapy (LTOT). LTOT may partly reverse hypoxic pulmonary vasoconstriction but is not always effective in reducing PAP in COPD. Patients with severe and persistent pulmonary hypertension despite oxygen and bronchodilator may be candidates for vasodilator therapy. Numerous vasodilators have been tested, but none has proved entirely satisfactory. Ideally the predominant vasodilator effect would occur in the pulmonary rather than in the systemic vascular bed, and systemic blood pressure should be maintained. The drug should not cause tachycardia and should be well tolerated. At the present time, inhaled nitric oxide (NO) is the only selective pulmonary vasodilator currently available, but NO inhalation is limited by toxicological consideration. Urapidil is known to be an alpha 1-adrenoceptor antagonist and an agonist of central 5HT1A-receptors, and should be considered as a vasodilator. Several studies have already demonstrated that this antihypertensive agent exerts favourable effects on pulmonary and cardiac haemodynamics when administered intravenously or orally to COPD patients with secondary pulmonary hypertension or cor pulmonale. Furthermore in patients with COPD or bronchial hyperreactivity no adverse effect is observed on ventilatory function, bronchial reactivity and gas exchange. Nevertheless, the potential benefit of this vasodilator needs to be confirmed in combination with LTOT by a pragmatic evaluation of its clinical efficacy and safety in COPD patients with secondary pulmonary hypertension.