Increased attention has been paid recently to the effect of diabetes on the pulmonary blood flow with indicating a dramatic growth in lung diseases and the possible association of diabetes with pulmonary arterial hypertension. Chronic hyperglycemia triggers a cascade of pathological reactions based on the oxidative stress stipulated by increase in number of the free electron donors with strengthening the electron stream in the mitochondrial electron transport chain. The numerous studies confirm an increase in concentration of the active oxygen forms in the pulmonary arteries as well in diabetes mellitus, so this mechanism may be regarded as an universal for both systemic and pulmonary circulation. The effects of hyperglycemia, namely oxidative stress, activation of the polyol and hexosamine pathways of glucose metabolism, activation of protein kinase with enhanced formation of the glycation final products increase the constricting capacity of the blood vessels in the greater circulation, but any effects of these factors on the blood vessels in the lesser circulation have been studied insufficiently. An expression of insulin receptors and glucose transporters has been revealed in the lung tissue, but virtually no data exist on their localization and density in the pulmonary artery wall, or any changes at the receptor or postreceptor levels in insulin resistance and diabetes mellitus.