title: [Effect of hypoxia on the conversion of angiotensin I to A II in pulmonary vascular endothelial cells].
abstract: The effect of hypoxia on intrapulmonary conversion of angiotensin I (A I) to angiotensin II (A II) was examined by using an isolated rat lung preparation perfused at constant flow and cultured calf pulmonary artery endothelial cells. The conversion rate of A I in endothelial cells of pulmonary vascular bed was found to be decreased in both acute hypoxic and chronic hypoxic (CH-5000, CH-8000) rats. The conversion rate of A I to A II was significantly higher in acute hypoxic rat lungs than that in denuded endothelial cells rat lungs. There was no significant difference between chronic hypoxic and denuded endothelial cells rat lungs. In cultured calf pulmonary artery endothelial cells (PAEC) exposed to hypoxia (3% O2) for 30 minutes the conversion of A I to A II was significantly reduced. In the time course of hypoxic exposure the conversion of A I to A II in cultured calf PAEC showed significant difference between hypoxia and normoxia. The results indicated that (1) Acute and chronic hypoxia impaired pulmonary conversion of A I to A II. (2) Effect of hypoxia on the pulmonary conversion of A I to A II is associated with the degree and the time of hypoxia.
authors.affiliation: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing.
authors.forename: B S
authors.initials: BS
authors.lastname: Qi
authors.forename: Y N
authors.initials: YN
authors.lastname: Cai
authors.forename: X X
authors.initials: XX
authors.lastname: Deng
authors.forename: S M
authors.initials: SM
authors.lastname: Zhou
mesh_terms: D000803:Angiotensin I / Q000378:metabolism*; D000804:Angiotensin II / Q000096:biosynthesis*; D000818:Animals; D015687:Cell Hypoxia; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D011651:Pulmonary Artery / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000804:Angiotensin II; D000803:Angiotensin I