The investigation were performed on 72 anaesthetized,immobilized and artificiallyrespired rabbits.Intrapulmonary arterial injection of 20～100 μg of histamine(HA)into the pul-monary artery causes an increase of the pulmonary arterial pressure and the carotid arterial pressureshowed either pressor and depressor as well as biphasec responses.The increase of pulmonary arterialpressure is accompained by a transient drop of the cardiac output without affecting the heart rate.The pressor response in the pulmonary and carotid arteries to HA could be blocked by H_1-receptor an-tagonist-chlorpheniramine and the depressor response to HA in caroti artery could be potentiated.Thederpessor response to HA in the carotid artery could be blocked and pressor response to HA in the pul-monary and carotid arteries could be potentiated by H_2-receptor antagonist-cimetidene.Simultaneousapplication of cimetidine and chlorpheniramine entirely abolish all the vascular response to HA inboth the pulmonary and carotid arteries.The vascular response in the pulmonary and carotid arteriesto HA was not affected by or-receptor antagonist-phentolmine and β-receptor antagonist-propranolon.The above results suggest in the intact rabbits the histamine-induced pressor response in the pul-monary artery is due to the vasoconstriction mediated by H_1-receptor and depressor response is due tovasodilation mediated by H_2-receptor.In normal physiological conditions,HA induces predominatlythe H1 receptor activety in pulmonary vassels. The investigations were performed on 72 anaesthetized, immobilized and artificiallyrespired rabbits. Intrapulmonary arterial injection of 20-100 μg of histamine (HA) into the pul-monary artery causes an increase of the pulmonary arterial pressure and the carotid arterial pressures were either pressedor and depressor as well as biphase responses. increase of pulmonary arterial pressure is accompained by a transient drop of the cardiac output without affecting the heart rate. pressor response in the pulmonary and carotid arteries to HA could be blocked by H_1 -receptor-tagonist-chlorpheniramine and the depressor response to HA in the caroti artery could be potentiated. Thederpessor response to HA in the carotid artery could be blocked and pressor response to HA in the pul-monary and carotid arteries could be potentiated by H_2-receptor antagonist-cimetidene. Simultaneous application of cimetidine and chlorpheniramine entirely abolish all the vascular response to HA inboth the pulmonary and carotid arteries. vascular response in the pulmonary and carotid arteriesto HA was not affected by or-receptor antagonist-phentolmine and beta-receptor antagonist-propranolon. The above results suggest in the intact rabbits the histamine-induced pressor response in the pul-monary artery is due to the vasoconstriction mediated by H_1 -receptor and depressor response is due tovasodilation mediated by H2_2 receptor. In normal physiological conditions, HA induces predominatly the H1 receptor activety in pulmonary vassels.