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ESTROGEN‐RESPONSIVE NEURONS IN THE MEDIAL AMYGDALA PREVENT STRESS‐INDUCED HYPERTENSION
Author(s) -
Hinton Antentor Othrell,
Xu Pingwen,
Yan Xiaofeng,
Reynolds Corey L.,
Xu Yong
Publication year - 2013
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.27.1_supplement.654.11
Subject(s) - estrogen receptor , estrogen , blood pressure , endocrinology , medicine , amygdala , cancer , breast cancer
Background Hypertension is the leading cause of cardiovascular disease worldwide. The etiology of essential hypertension is unknown. Psychological stress contributes to development of hypertension in humans. Estrogen has been shown to prevent stress‐induced hypertension in rodents with unknown mechanisms. Amygdala neurons have been implicated in controlling blood pressure. Abundant estrogen receptors, including estrogen receptor‐α (ERα), are expressed in the medial amygdala (MeA). Thus, we hypothesize that ERα expressed by MeA neurons mediates the anti‐hypertensive effects of estrogen during stress. Methods We use the Cre‐LoxP system to remove ERα from specific MeA neurons in mice (ERαlox/lox/SIM1‐Cre). Female ERαlox/lox/SIM1‐Cre mice and controls (ERαlox/lox) were subjected to bilateral ovariectomy (OVX), given a vehicle (V) or 17‐β‐Estradiol pellet (E2), and inserted with telemetry probes on day one. After a seven‐day recovery, blood pressure was recorded for 3 hours to establish baseline and then mice were subjected to 1 hour stress restraint. Results ERαlox/lox OVX + V mice showed increased mean arterial blood pressure (MAP) and systolic arterial blood pressure (SAP) in response to stress, whereas this stress‐induced hypertension was blunted in ERαlox/lox OVX + E mice. Interestingly, ERαlox/lox/SIM1‐Cre OVX + E and OVX + V group both showed increased MAP and SAP in response to stress. Conclusions Our results suggest that ERα in the MeA is required to mediate estrogenic actions to prevent stress‐induced hypertension.