ArticleAmerican journal of physiology. Heart and circulatory physiology2005
Estrogen-induced contraction of coronary arteries is mediated by superoxide generated in vascular smooth muscle.
Article in American journal of physiology. Heart and circulatory physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Prevalence of hypertension in adults living at altitude in Latin America and the Caribbean: A systematic review and meta-analysis.PloS one · 2023Pooled it
- Diabetes Type 2 in Women: The Impact of EndogenousOestrogen, A Population-Based Study With About 2 Decades of Follow-Up.Endocrinology, diabetes & metabolism · 2026Article
- Bitter taste receptor agonists induce vasorelaxation in porcine coronary arteries.Frontiers in pharmacology · 2025Article
- Endogenous estradiol contributes to vascular endothelial dysfunction in premenopausal women with type 1 diabetes.Cardiovascular diabetology · 2023Article
- Mechanisms and clinical implications of endothelium-dependent vasomotor dysfunction in coronary microvasculature.American journal of physiology. Heart and circulatory physiology · 2022Review
- Estrogen signaling as a bridge between the nucleus and mitochondria in cardiovascular diseases.Frontiers in cell and developmental biology · 2022Review
- An autophagic deficit in the uterine vessel microenvironment provokes hyperpermeability through deregulated VEGFA, NOS1, and CTNNB1.Autophagy · 2021Article
- Restoration of Adiponectin-Connexin43 Signaling Mitigates Myocardial Inflammation and Dysfunction in Diabetic Female Rats.Journal of cardiovascular pharmacology · 2020Article
- Lymphatic Function and Dysfunction in the Context of Sex Differences.ACS pharmacology & translational science · 2019Review
- Estrogen-Dependent Disruption of Adiponectin-Connexin43 Signaling Underlies Exacerbated Myocardial Dysfunction in Diabetic Female Rats.The Journal of pharmacology and experimental therapeutics · 2019Article
- The protective role of estrogen and estrogen receptors in cardiovascular disease and the controversial use of estrogen therapy.Biology of sex differences · 2017Review
- Article
- Menopause and Ischemic Stroke: A Brief Review.MOJ toxicology · 2017Article
- Effects of estrogen on cerebrovascular function: age-dependent shifts from beneficial to detrimental in small cerebral arteries of the rat.American journal of physiology. Heart and circulatory physiology · 2016Article
- Estrogen receptor ERα plays a major role in ethanol-evoked myocardial oxidative stress and dysfunction in conscious female rats.Alcohol (Fayetteville, N.Y.) · 2016Article
- Delonix regia Leaf Extract (DRLE): A Potential Therapeutic Agent for Cardioprotection.PloS one · 2016Article
- G-protein-coupled estrogen receptor as a new therapeutic target for treating coronary artery disease.World journal of cardiology · 2014Review
- Peroxynitrite mediates testosterone-induced vasodilation of microvascular resistance vessels.The Journal of pharmacology and experimental therapeutics · 2013Article
- Protective cardiovascular and renal actions of vitamin D and estrogen.Frontiers in bioscience (Scholar edition) · 2013Review
- Enhanced vascular neuronal nitric-oxide synthase-derived nitric-oxide production underlies the pressor response caused by peripheral N-methyl-D-aspartate receptor activation in conscious rats.The Journal of pharmacology and experimental therapeutics · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Although previous studies demonstrated beneficial effects of estrogen on cardiovascular function, the Women's Health Initiative has reported an increased incidence of coronary heart disease and stroke in postmenopausal women taking hormone replacement therapy. The objective of the present study was to identify a molecular mechanism whereby estrogen, a vasodilatory hormone, could possibly increase the risk of cardiovascular disease. Isometric contractile force recordings were performed on endothelium-denuded porcine coronary arteries, whereas molecular and fluorescence studies identified estrogen signaling molecules in coronary smooth muscle. Estrogen (1-1,000 nM) relaxed arteries in an endothelium-independent fashion; however, when arteries were pretreated with agents to uncouple nitric oxide (NO) production from NO synthase (NOS), estrogen contracted coronary arteries with an EC(50) of 7.3 +/- 4 nM. Estrogen-induced contraction was attenuated by reducing superoxide (O(2)(-)). Estrogen-stimulated O(2)(-) production was detected in NOS-uncoupled coronary myocytes. Interestingly, only the type 1 neuronal NOS isoform (nNOS) was detected in myocytes, making this protein a likely target mediating both estrogen-induced relaxation and contraction of endothelium-denuded coronary arteries. Estrogen-induced contraction was completely inhibited by 1 muM nifedipine or 10 muM indomethacin, indicating involvement of dihydropyridine-sensitive calcium channels and contractile prostaglandins. We propose that a single molecular mechanism can mediate the dual and opposite effect of estrogen on coronary arteries: by stimulating type 1 nNOS in coronary arteries, estrogen produces either vasodilation via NO or vasoconstriction via O(2)(-).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.