the ras has an important role in the control of body fluid , electrolyte balance and arterial pressure . estrogen activates the synthesis of the rennin substrate angiotensinogen and it inhibits plasma renin activity . it is reported that estrogen administration in ovarectomised rats is caused upregulation of angiotensin type 2 receptor ( at2r ) , and angiotensin ii ( angii ) is caused a stronger vasoconstriction in ovarectomised rats . nitric oxide ( no ) is an endogenous mediator in different biological actions including vasodilation . it also was reported that no releasing was significantly higher in ovarectomised rats treated with estradiol ( ove ) and estrogen induces augmentation of no production through vascular endothelium . so , with attention to role of estrogen in at2r expression and no releasing , in this study we attempt to find the role of estrogen on no releasing in response to angii in presence and absence of at2r in female rats . the rats were housed at a temperature of 23 - 25c with a 12 h light / dark cycle and they had free access to water rat chow . the experimental groups were as ( 1 ) intact animals ; ( 2 ) ovariectomised rats treated with placebo for 2 weeks ( ovx ) , and ( 3 ) ove valerate ( 0.5 mg / kg body weight , i.m ) for 2 week ( ove ) . louis usa ) , trachea was isolated to insert air ventilation tube and catheters were implanted into the carotid artery and jugular vein . blood pressure was monitor through carotid artery and after the equilibration period , rats from each group were divided into two subgroups . one subgroup received saline vehicle ( 0.9% saline ) and the other subgroup received at2r antagonist ; pd123319 ( sigma , st . louis , mo , usa , 1 mg / kg as bolus plus continuous infusion of 1 mg / kg / h during the experiment ) . at 30 min after commencing vehicle or antagonists treatments , intravenous infusions angii ( 20 g / kg / h ) for period of 60 min commenced . the blood samples also were obtained before and after the angii infusion for nitrite concentration determination . the level of nitrite was measured using a colorimetric assay kit ( promega corporation , usa ) that involves the griess reaction . the serum level of nitrite before ( control ) and after ( treat ) angii infusion between the groups were compared via repeated measures anova with factors group ( intact , ovx and ove ) and time ( before and after angii infusion ) and their interaction . the serum level of nitrite before ( control ) and after ( treat ) angii infusion between the groups were compared via repeated measures anova with factors group ( intact , ovx and ove ) and time ( before and after angii infusion ) and their interaction . the results are presented in figure 1a and b. at control phase ( before angii administration ) , no significant differences were observed between the subgroups neither treated with vehicle nor pd123319 . after angii administration when at2r antagonist ( pd123319 ) was not infused , the serum level of nitrite in response to angii administration in ove groups increased significantly [ figure 1a ] ( p < 0.05 ) . however , this increase was abolished by at2r antagonist [ figure 1b ] . the serum level of nitrite in three groups of experiments before ( control ) and after ( treat ) angiotensin ii administration without ( a ) and with ( b ) antagonist ; pd123319 . significant difference was observed between estradiol and other groups when angiotensin type 2 receptor was present . star ( * ) indicate significant difference from others group ( p < 0.05 ) . ovx ; ovariectomised rats treated with placebo , ove ; ovariectomised rats treated with estradiol , and n in the top legend shows the number of animal in each subgroups the results are presented in figure 1a and b. at control phase ( before angii administration ) , no significant differences were observed between the subgroups neither treated with vehicle nor pd123319 . after angii administration when at2r antagonist ( pd123319 ) was not infused , the serum level of nitrite in response to angii administration in ove groups increased significantly [ figure 1a ] ( p < 0.05 ) . however , this increase was abolished by at2r antagonist [ figure 1b ] . the serum level of nitrite in three groups of experiments before ( control ) and after ( treat ) angiotensin ii administration without ( a ) and with ( b ) antagonist ; pd123319 . significant difference was observed between estradiol and other groups when angiotensin type 2 receptor was present . star ( * ) indicate significant difference from others group ( p < 0.05 ) . ovx ; ovariectomised rats treated with placebo , ove ; ovariectomised rats treated with estradiol , and n in the top legend shows the number of animal in each subgroups in this short study , we found that the serum level of nitrite increased significantly after angii administration in ove group when at2r is present , and this increase was abolished by at2r antagonist . estrogen is responsible of complex effects on ras components and there is interaction between estrogen and at2r . at2r activation opposes with at1r actions and estrogen decreases at1r / at2r ratio . confirmed with our result other studies have reported that ovariectomised rats treated with estrogen is caused enhancing endothelium derived relaxing factor level due to increasing of endothelial no synthase . the vasodilatory effect of estrogen response to angii administration may mediate by at2r to increase the serum level of no metabolite in female rats . due to gender difference of angii receptors activities , the role of at2r in no formation response to angii infusion may be different in male .