Ontology highlight
ABSTRACT: Background
We documented the dependence of ethanol (EtOH)-evoked myocardial dysfunction on estrogen (E2 ), and our recent estrogen receptor (ER) blockade study, in proestrus rats, implicated ERα signaling in this phenomenon. However, a limitation of selective pharmacological loss-of-function approach is the potential contribution of the other 2 ERs to the observed effects because crosstalk exists between the 3 ERs. Here, we adopted a "regain"-of-function approach (using selective ER subtype agonists) to identify the ER subtype(s) required for unraveling the E2 -dependent myocardial oxidative stress/dysfunction caused by EtOH in conscious ovariectomized (OVX) rats.Methods
OVX rats received a selective ERα (PPT), ERβ (DPN), or GPER (G1) agonist (10 μg/kg
SUBMITTER: Yao F
PROVIDER: S-EPMC5272804 | biostudies-literature | 2017 Feb
REPOSITORIES: biostudies-literature