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 .
 background : renin - angiotensin system activity is gender related . 
 the vasodilatory response of angiotensin ii ( angii ) angiotensin type 2 receptor ( at2r ) may involve nitric oxide ( no ) production . 
 we attempted to find the role of at2r on no formation response to angii administration in ovariectomised rats treated with estradiol ( ove).methods : a total of 33 female wistar rats were divided into 3 groups ; intact animals , ovariectomised treated with placebo ( ovx ) and ove . at 2 weeks later , all animals were subjected to anesthetize and catheterize and each group was divided into two subgroups that received at2r antagonist ( pd123319 ) or vehicle . 
 each animal was subjected to 1 h continuous infusion of angii ( ~20 g / kg / h ) and the level of no metabolite ( nitrite ) was measured before and after angii infusion.results:at the presence of at2r , the serum level of nitrite in response to angii administration in ove groups increased significantly ( p < 0.05).conclusions : however , this increase was abolished by at2r antagonist . 
 it seems that at2r involves nitrite production response to angii in ove . 
INTRODUCTION
METHODS
Statistical analysis
RESULTS
Serum nitrite concentration
DISCUSSION
CONCLUSIONS