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Central estrogen attenuates Ang II‐induced hypertension in ovariectomized female mice
Author(s) -
Xue Baojian,
Johnson Ralph F,
Beltz Terry,
Johnson Alan Kim,
Hay Meredith
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb37
Subject(s) - ovariectomized rat , medicine , endocrinology , estrogen , blood pressure , ventricle , estrogen receptor , antagonist , receptor , chemistry , cancer , breast cancer
It has been shown that ovariectomy (OVX) exacerbates high blood pressure (BP), that estrogen replacement attenuates the course of hypertension, and that estrogen acts on several central nuclei involved in cardiovascular regulation. The present study tested the effects of central estrogen and its receptors on Ang II induced hypertension. Aortic BP was measured in conscious female mice with the use of telemetry implants. In OVX females 17β‐estradiol (E2, 30 μg/kg/day, n=5) or E2 plus an estrogen receptors antagonist (ICI182,780,10 μM, n=5) were chronically infused into lateral ventricle by brain infusion assembly with attached osmotic pump. AngII(800 ng/kg/min) was infused subcutaneously via an osmotic pump. Resting BPs were similar in intact and OVX mice. After 7 days of systemic infusion, Ang II resulted in only 7.2± 2.0 mmHg increase in BP in intact mice (n=7, 102.4±1.1 to 114.2±2.5mmHg). But in OVX mice, Ang II increased significantly BP by 23±1 mmHg (n=5, 99.2±0.9 to 122.4±1.4 mmHg). Central infusions of E2, or E2+ICI182,780 did not change the basal BP. However, central infusion of E2 attenuated the pressor effect of Ang II (Δ MAP 7±0.4 mmHg n=4). This protective effect of E2 was prevented by co‐administration of ICI(Δ MAP 18.8±1.5 mmHg n=4). Finally, ganglionic blockade on day 7 after beginning the Ang II infusions resulted in greater reduction in BP in OVX females administered E2+ICI centrally(−60.1±5.2 mmHg) as compared with OVX mice given just central E2 (−39.8±3.5 mmHg). This suggests a role for the sympathetic nervous system in this response. Taken together these results suggest central estrogen and/or its receptors may play a protective role in development of Ang II‐induced hypertension in female mice. (Supported by NIH Grant 62261 and 59676)