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MEDIATES ESTROGEN PROTECTION FROM ANGIOTENSIN II-INDUCED HYPERTENSION IN CONSCIOUS FEMALE MICE
1 Department of Psychology, University of Iowa, Iowa City, Iowa, United States
2 Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Missouri, United States
3 University of Missouri Center for Phytonutrient and Phytochemical Studies, University of Missouri-Columbia, Columbia, Missouri, United States
4 Department of Physiolgy & Biophysics, University of Iowa, Iowa City, Iowa, United States; Department of Psychology, University of Iowa, Iowa City, Iowa, United States
* To whom correspondence should be addressed. E-mail: baojian-xue{at}uiowa.edu.
It has been shown that the female sex hormones have a protective role in the development of Angiotensin II (ANG II) induced hypertension. The present study tested the hypotheses that 1) the estrogen receptor alpha (ER
) is involved in the protective effects of estrogen against ANG II induced hypertension and 2) that central ER are involved. Blood pressure (BP) was measured in female mice with the use of telemetry implants. ANG II (800 ng/kg/min) was administered subcutaneously via an osmotic pump. Baseline BP in the intact, Ovariectomized (OVX) wild type (WT) and ER KO mice were similar, however the increase in BP induced by ANG II was greater in OVX WT (23.0± 1.0 mmHg), ER KO mice (23.8± 2.5 mmHg) than in intact WT mice (10.1± 4.5 mmHg). In OVX WT mice, central infusion of E2 (30 µg/kg/d) attenuated the pressor effect of ANG II (7.0± 0.4 mmHg), and this protective effect of E2 was prevented by co-administration of ICI182,780, a nonselective antagonist (ICI, 1.5 µg/kg/d, 18.8 ±1.5 mmHg). Furthermore, central (but not peripheral) infusions of ICI augmented the pressor effects of Ang II in intact WT mice (17.8 ±4.2 mmHg). In contrast, the pressor effect of ANG II was unchanged in either central E2 treated OVX ERKO mice (19.0±1.1 mmHg) or central ICI treated intact ERKO mice (19.6±1.6 mmHg). Lastly, ganglionic blockade on day 7 after Ang II infusions resulted in greater reduction in BP in OVX WT, central ER antagonist treated intact WT, central E2+ICI treated OVX WT, ER KO and central E2 or ICI treated ERKO mice as compared with intact WT mice given just ANG II. Together, these data indicate that ER , especially central expression of the ER, mediates the protective effects of estrogen against Ang II induced hypertension.
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