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knockout mice
1 Div. of Obstetrics and Gynaecology, Karolinska Institutet, Institution for Clinical Science, Intervention and Technology, Stockholm, Sweden
2 Div. of Reproductive Health, Endocrinology and Development, Kings College London, Maternal and Fetal Research Unit, London, United Kingdom
3 Dept of Medical Nutrition, Karolinska Institutet, Stockholm, Sweden
* To whom correspondence should be addressed. E-mail: Karolina.Kublickiene{at}klinvet.ki.se.
Objectives: To determine if acute dilatory responses to estrogen receptor agonists are altered in isolated arteries from estrogen receptor 
deficient mice (ERKO), and to gain insight into the role of nitric oxide (NO) in these responses.
Methods: Femoral arteries (
250µm) from male and female ERKO mice and WT littermates (26 female, 13 in each group; and 24 male, 12 in each group) were mounted on a Multi-Myograph. Concentration-response curves to 17-estradiol (17-E2), and the selective ER
agonist Propyl-[1H]-pyrazole-1,3,5-triyl trisphenol (PPT) were obtained before and after NO synthase inhibition (N(G)-nitro-L-arginine methyl ester; L-NAME,0.1mM)in arteries preconstricted with U46619 (a thromboxane analogue). In WT mice, responses to the potent ER agonist 2,3-bis (4-Hydroxyphenyl)-propionitrile (DPN) and the contribution of NO were also assessed.
Results: Concentration response curves to 17-E2 and PPT were similar in arteries from WT and ERKO mice of both genders, but NO mediated relaxation was different as L-NAME reduced 17-E2 mediated relaxation in arteries from male and female ERKO but not WT mice (p<0.05). NOS-inhibition reduced dilation to PPT in arteries from male and female WT mice, as well as arteries from female ERKO mice (p<0.05). Responses to DPN in arteries from WT female and male mice did not differ after NOS-inhibition.
Conclusion: The acute dilatory responses to estrogenic compounds are similar in WT and ERKO mice, but differ mechanistically. As NO appeared to contribute to responses to 17-E2 in arteries from ERKO but not WT mice, the presence of ER apparently inhibits ER mediated NO relaxation.
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