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knockout mice
Karolinska Institutet, 1Institution for Clinical Science, Intervention, and Technology, Division of Obstetrics and Gynecology and 3Department of Medical Nutrition, Karolinska University Hospital, Huddinge, Stockholm, Sweden; and 2Maternal and Fetal Research Unit, Division of Reproductive Health, Endocrinology, and Development, Kings College London, London, United Kingdom
Submitted 1 August 2005 ; accepted in final form 19 September 2005
The objectives of this study were to determine whether 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. Femoral arteries (
250 µm) from male and female -ERKO mice and wild-type (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 estrogen receptor-
(ER-) agonist propyl-[1H]-pyrazole-1,3,5-triy-trisphenol (PPT) were obtained before and after NO synthase (NOS) inhibition [N
-nitro-L-arginine methyl ester (L-NAME), 0.1 mM] in arteries preconstricted with U-46619 (a thromboxane analog). In WT mice, responses to the potent estrogen receptor- (ER-) agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) and the contribution of NO were also assessed. 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, since 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. The acute dilatory responses to estrogenic compounds are similar in WT and -ERKO mice but differ mechanistically. Because 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.
femoral arteries; estrogen receptor knockout mice; vasodilation; propyl-[1H]-pyrazole-1,3,5-triy-trisphenol; nitric oxide
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