ArticleAlcohol (Fayetteville, N.Y.)2016
Estrogen receptor ERα plays a major role in ethanol-evoked myocardial oxidative stress and dysfunction in conscious female rats.
Article in Alcohol (Fayetteville, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Sex Difference of Alcoholic Hypertension: Mechanism and Targeted Therapy.Current hypertension reports · 2025Review
- Estrogen replacement restores period 2-mediated inhibition of ferroptosis and mitigates cardiac dysfunction in estrogen-deficient rats.The Journal of pharmacology and experimental therapeutics · 2025Article
- Study on the In Vitro and In Vivo Antioxidant Activity and Potential Mechanism ofAntioxidants (Basel, Switzerland) · 2025Article
- Ethanol-induced lung and cardiac right ventricular inflammation and remodeling underlie progression to pulmonary arterial hypertension.Alcohol, clinical & experimental research · 2024Article
- Heart Failure in Menopause: Treatment and New Approaches.International journal of molecular sciences · 2022Review
- Ethanol Metabolism in the Liver, the Induction of Oxidant Stress, and the Antioxidant Defense System.Antioxidants (Basel, Switzerland) · 2022Review
- The protective effects of 17-β estradiol and SIRT1 against cardiac hypertrophy: a review.Heart failure reviews · 2022Review
- Tetrahydrobiopterin paradoxically mediates cardiac oxidative stress and mitigates ethanol-evoked cardiac dysfunction in conscious female rats.European journal of pharmacology · 2021Article
- Sex Differences in the Vasodilation Mediated by G Protein-Coupled Estrogen Receptor (GPER) in Hypertensive Rats.Frontiers in physiology · 2021Article
- Alcohol suppresses cardiovascular diurnal variations in male normotensive rats: Role of reduced PER2 expression and CYP2E1 hyperactivity in the heart.Alcohol (Fayetteville, N.Y.) · 2020Article
- Estrogen-dependent hypersensitivity to diabetes-evoked cardiac autonomic dysregulation: Role of hypothalamic neuroinflammation.Life sciences · 2020Article
- Aldehyde Dehydrogenase Inhibition Ameliorates Cardiac Dysfunction and Exacerbates Hypotension Caused by Alcohol in Female Rats.Alcoholism, clinical and experimental research · 2020Article
- Role of Alcohol Oxidative Metabolism in Its Cardiovascular and Autonomic Effects.Advances in experimental medicine and biology · 2019Review
- Combined Catalase and ADH Inhibition Ameliorates Ethanol-Induced Myocardial Dysfunction Despite Causing Oxidative Stress in Conscious Female Rats.Alcoholism, clinical and experimental research · 2017Article
- Estrogen receptor α activation enhances its cell surface localization and improves myocardial redox status in ovariectomized rats.Life sciences · 2017Article
- Evidence of Altered Mitochondrial Protein Expression After Chronic Ethanol Consumption in the Aged Estrogen-Deficient Female Rat Heart.Alcoholism, clinical and experimental research · 2017Article
- Influence of sex on cardiovascular drug responses: role of estrogen.Current opinion in pharmacology · 2017Review
- Estrogen Receptors α and β Play Major Roles in Ethanol-Evoked Myocardial Oxidative Stress and Dysfunction in Conscious Ovariectomized Rats.Alcoholism, clinical and experimental research · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Our previous studies showed that ethanol elicited estrogen (E2)-dependent myocardial oxidative stress and dysfunction. In the present study we tested the hypothesis that E2 signaling via the estrogen receptor (ER), ERα, mediates this myocardial detrimental effect of alcohol. To achieve this goal, conscious female rats in proestrus phase (highest endogenous E2 level) received a selective ER antagonist (200 μg/kg; intra-venous [i.v.]) for ERα (MPP), ERβ (PHTPP) or GPER (G15) or saline 30 min before ethanol (1 g/kg; i.v.) or saline infusion. ERα blockade virtually abrogated ethanol-evoked myocardial dysfunction and hypotension, while ERβ blockade had little effect on the hypotensive response, but caused delayed attenuation of the ethanol-evoked reductions in left ventricular developed pressure and the rate of left ventricle pressure rise. GPER blockade caused delayed attenuation of all cardiovascular effects of ethanol. All three antagonists attenuated the ethanol-evoked increases in myocardial catalase and ALDH2 activities, Akt, ERK1/2, p38, eNOS, and nNOS phosphorylation, except for a lack of effect of PHTPP on p38. Finally, all three ER antagonists attenuated ethanol-evoked elevation in myocardial ROS, but this effect was most notable with ERα blockade. In conclusion, ERα plays a greater role in, and might serve as a molecular target for ameliorating, the E2-dependent myocardial oxidative stress and dysfunction caused by ethanol.
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