Abstract: Objective:The regulative effects of genistein on vascular active factors, to find its mechanism to suppressed pulmonary hypertension and vascular structural remodeling, were discussed in chronic hypoxic rats. Methods: Male Wistar ratswere randomly divided into control group (C), hypoxia group (H) and hypoxia with genistein group (H+G). Control group of rats was kept in cages exposed to room air. H and (H+G) groups of rats were exposed to 21 days of hypobaric hypoxia(simulate altitude 5000m)for 8h everyday. During their esposure to hypoxia, rats were i.g. administered once a day with solvent or phytoestrogens. The levels of nitric oxide(NO), endothelin (ET-1), prostacyclin (PGI2), 17β-estradiol (E2), superoxide dismutase(SOD) and malondialdehyde (MDA) of blood were measured. Results: Genistein could increase NO and PGI2, and decrease ET-1 levels and also be responsible for genistein induced vasodilation. In addition, genistein could increase the activity of SOD and inhibit MDA product. Serum 17β-estradiol levels were not significantly different among rats in three groups. Conclusions: Genistein could suppress SMC proliferation by inhibiting the synthesis and secretion of ET-1 and other SMC proliferation-promoting factors, and enhancing the synthesis and secretion of SMC proliferation-inhibitory factors, such as NO and PGI2. Genistein did not have the side effects, such as feminizing and oncogenic effects, of the estrogens.

Key words: genistein, hypoxia, nitric oxide, endothelin, prostacyclin