Calcium ion acts as a second messenger in numerous cellular functions. The increase in its intracellular free concentration, which is brought about by influx from the extracellular source through voltage-dependent or receptor-operated channels and/or by release from intracellular sources, triggers the contraction of smooth muscle. The currently available calcium antagonists inhibit calcium movement through voltage-dependent channels. Tracheobronchial and pulmonary vascular smooth muscles play an important role in the symptomatic expression of chronic airflow obstruction. Whether an alteration in their functioning is involved in the pathogenic mechanism of the disease has not yet been established. The contraction of bronchial smooth muscle participates in bronchial obstruction and that of vascular muscle in pulmonary arterial hypertension, which complicates hypoxemic airflow obstruction. Numerous clinical and experimental studies show that bronchodilator or anti-bronchoconstrictor effects of calcium antagonists are limited. This limitation may be linked to either a low affinity of calcium antagonists for bronchial smooth muscle or a specificity of the mechanism of excitation-contraction coupling in this muscle. Calcium antagonists are powerful inhibitors of hypoxic pulmonary vasoconstriction. This inhibition may lead to a worsening of hypoxemia in relation to redistribution of blood flow towards low ventilation/perfusion ratio areas although the concomitant rise in cardiac output leads to increased oxygen transport. These effects seem to be maintained in the long term.