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Estrogen receptor- mediates estrogen protection from angiotensin II-induced hypertension in conscious female mice

Departments of ¹Physiology and Biophysics and ²Psychology, University of Iowa; Iowa City, Iowa; and ³Dalton Cardiovascular Research Center and ⁴University of Missouri Center for Phytonutrient and Phytochemical Studies, University of Missouri-Columbia, Columbia, Missouri

Submitted 22 September 2005 ; accepted in final form 22 November 2006

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- (ER) is involved in the protective effects of estrogen against ANG II-induced hypertension and 2) central ERs are involved. Blood pressure (BP) was measured in female mice with the use of telemetry implants. ANG II (800 ng·kg^–1·min^–1) was administered subcutaneously via an osmotic pump. Baseline BP in the intact, ovariectomized (OVX) wild-type (WT) and ER knockout (ERKO) mice was similar; however, the increase in BP induced by ANG II was greater in OVX WT (23.0 ± 1.0 mmHg) and ERKO mice (23.8 ± 2.5 mmHg) than in intact WT mice (10.1 ± 4.5 mmHg). In OVX WT mice, central infusion of 17-estradiol (E₂; 30 µg·kg^–1·day^–1) attenuated the pressor effect of ANG II (7.0 ± 0.4 mmHg), and this protective effect of E₂ was prevented by coadministration of ICI-182,780 (ICI; 1.5 µg·kg^–1·day^–1, 18.8 ± 1.5 mmHg), a nonselective ER antagonist. 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 a greater reduction in BP in OVX WT, central ER antagonist-treated intact WT, central E₂ + ICI-treated OVX WT, ERKO, and central E₂- or ICI-treated ERKO mice compared with that in 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.

cardiovascular disease; sex hormone

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