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Estrogen Receptor-α in the Medial Amygdala Prevents Stress-Induced Elevations in Blood Pressure in Females
Antentor Othrell Hinton1, Yanlin He1, Yan Xia1
1From the Department of Pediatrics, Children's Nutrition Research Center (A.O.H., Y.H., Y.X., P.X., Y.Y., K.S., C.W., X.Y., G.S., A.H., Q.W., Y.X.), Advanced Technology/Core Laboratory (C.R.), and Department of Molecular and Cellular Biology (Y.X.), Baylor College of Medicine, One Baylor Plaza, Houston, TX; Department of Biomedical Research, Diabetes and Obesity Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA (D.J.C.); Department of Cell and Cancer Biology, Vontz Center for Molecular Studies, University of Cincinnati, College of Medicine, OH (S.A.K.); and Center for Metabolic and Degenerative Diseases, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston (Q.T.).
Abstract:
Psychological stress contributes to the development of hypertension in humans. The ovarian hormone, estrogen, has been shown to prevent stress-induced pressor responses in females by unknown mechanisms. Here, we showed that the antihypertensive effects of estrogen during stress were blunted in female mice lacking estrogen receptor-α in the brain medial amygdala. Deletion of estrogen receptor-α in medial amygdala neurons also resulted in increased excitability of these neurons, associated with elevated ionotropic glutamate receptor expression. We further demonstrated that selective activation of medial amygdala neurons mimicked effects of stress to increase blood pressure in mice. Together, our results support a model where estrogen acts on estrogen receptor-α expressed by medial amygdala neurons to prevent stress-induced activation of these neurons, and therefore prevents pressor responses to stress.
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