The roles of sympathicus, sensory neuropeptides (SNP), cyclooxygenase metabolites (COX-M), lipoxygenase metabolites (LOX-M), endothelium derived relaxing factor (EDRF), reactive oxygen (ROS) and potassium channels (PC) in the hypoxic pulmonary vasoconstriction (HPV) and hypoxic cerebral vasodilation (HCVD) were investigated in intact rats, rabbits and dogs. The results showed that during hypoxia, the excitation of sympathicus caused a constriction of both pulmonary and cerebral vessels, while SNP, EDRF and the opening of voltage sensitive PC caused the dilation of both of them; LOX-M mediated HPV and HCVD, COX-M might serve as their modulators; the blockade of ATP sensitive PC induced by hypoxia mediated HPV, but had no effect on HCVD; the reduction of O2-. in the lung might potentiate HPV, however, O2-. remained unchanged in brain during hypoxia. It is suggested that the alterations of LOX-M, ROS and the ATP sensitive PC are the factors accounting for the difference in the response of pulmonary and cerebral vessels to hypoxia.