The alteration in hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking was studied in Wistar rats, piglets and in humans. The percentage change of pulmonary vascular resistance (delta PVR%) and the amplitude of the systolic wave in impedance pneumorheogram (delta H%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats increased (delta PVR% from 55.0 +/- 15.6% to 102.3 +/- 12.4%), which is mainly mediated by leukotrienes (LTs); whereas HPV in piglets decreased (delta PVR% from 65.2 +/- 12.5% to 55.9 +/- 9.8%), which is mainly mediated by beta-adrenergic receptors, and HPV in humans also increased (delta H% from 20.6 +/- 2.6% to 31.1 +/- 4.1%), in which prostaglandins and leukotrienes may play the role of mediators. However, after one-month cigarette smoking, the HPV in rats fell significantly (delta PVR% 11.4 +/- 1.6%). An increase in synthesis of vasodilative prostaglandins and a decrease in leukotrienes synthesis may be the contributing factors to this alteration in HPV.