title: [Role of gasotransmitters in the pathogenesis of pulmonary hypertension].
abstract: Pulmonary hypertension is a complicated and important pathological process in the development of a variety of cardiovascular and pulmonary diseases, and directly affects the development of the diseases and their prognosis. but its mechanisms are still not fully understood. Therefore, to clarify the mechanisms is an important task in this field. Nitric oxide (NO) and carbon monoxide (CO) have special significance in pulmonary circulation as compared with other organs for their special biological properties including continuous production, fast transmission and extensive action, etc, which attracts great attention in the life science research and initiates the new research field of gasotransmitters. Hydrogen sulfide (H2S), which has been recognized as a toxic gas, can be endogenously produced in the body. We considered it to be a new cardiovascular regulatory gasotransmitter based on the studies of its synthesis and distribution in cardiovascular system and cardiovascular effects under physiologic and pathophysiologic conditions. We found it exerted a general regulatory significance in cardiovascular diseases. Based on the research of the three gasotransmitters in hypoxic and high pulmonary blood flow-induced pulmonary hypertension, it was found that the dysfunction of the gasotransmitter pathways was involved in the pathogenesis of pulmonary hypertension and the supplement of gasotransmitters could alleviate pulmonary hypertension and pulmonary vascular remodeling. The mechanisms included that they could regulate vessel dilation, correct the imbalance between smooth muscle cell proliferation and apoptosis, inhibit the excess synthesis and stimulate the degradation of collagen, therefore inhibiting abnormal accumulation of collagen, etc. All these results indicated the significant regulatory effects of gasotransmitters in the pathogenesis of pulmonary hypertension.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
authors.forename: Yan-fei
authors.initials: YF
authors.lastname: Wang
authors.forename: Hong-fang
authors.initials: HF
authors.lastname: Jin
authors.forename: Chao-shu
authors.initials: CS
authors.lastname: Tang
authors.forename: Jun-bao
authors.initials: JB
authors.lastname: Du
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity; D002248:Carbon Monoxide / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D006862:Hydrogen Sulfide / Q000378:metabolism*; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D000860:Hypoxia / Q000150:complications / Q000378:metabolism; D008168:Lung / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism* / Q000502:physiology; D011652:Pulmonary Circulation; D051381:Rats
chemical_list: D009569:Nitric Oxide; D002248:Carbon Monoxide; D006862:Hydrogen Sulfide