Effects Of Estrogen And Progesterone On Platelet Aggregation,Nitric Oxide And Nitric Oxide Synthases Activity In Ovariectomized Rats

Objective: Through investigating the effect of chronic estrogen, progestogen and combined hormone replacement on serum nitric oxide (nitrite/nitrate) levels and rnyocardial nitric oxide synthase activity in ovariotomized rats, we study the protective mechanism of 1-IRT on cardiovascular system in postmenopausal women. Methods: Sixty female mature Sprague-Dawley rats were randomly divided into 8 groups: OVX group, OVX+vehicle group, OVX+E(1) group, OVX-1-E(2) group, OVX+P group, OVX+E+P group, sham OVX group and normal control group. The front six groups rats were subjected to ovariotomy, their E2 levels were measured at the end of the 4th week after ovariotomy to affirm the endogenous sex hormone deficiency rat model established and then they were treated with either vehicle (100 it 1 corn oil ), low dose estrogen , moderate dose estrogen, progestogen, or low dose estrogen and progestogen 12 weeks. At the end of the 16th week, the serum F2 and P levels were determined by radioimmunoassay, the platelet aggregation were measure by Born turbidity method, serum nitric oxide (nitrite /nitrate) levels and myocardial nitric oxide synthase activity were determined. Results: The serum F2 level and E2/P ratio showed positive correlation with serum nitric oxide and myocardial nitric oxide synthase activity, and showed negative correlation with the platelet aggregation, but the serum P level did not show correlation with them. For the OVX group rats, the platelet aggregation increased, serum nitric oxide level and myocardial nitric oxide synthase activity droped with serum E, level and E2/P ratio at the end of 16th week after ovariotomy. Progeslogen increased platelet aggregation, did not promote the serum nitric oxide levels and myocardial nitric oxide synthase activity and attenuated the beneficial effects of estrogen in the OVX+E+P group. The platelet aggregation decreased, serum nitric oxide level and myocardial nitric oxide synthase activity increased significantly in the OVX+E(1) group and OVX+E(2) group rats. Conclusion: Our study indicated that the cardiovascular protective mechanism of estrogen might include decreasing the platelet aggregation, increasing nitric oxide production or volume released from endothelium, and improving nitric oxide synthase activity, and these effects of estrogen were correlated with the serum E2 level and E2/P ratio. The higher rats of CHD in postmenopausal women maybe due to the estrogen level decreasing and E2/P ratio abnormal.