ArticleThe Journal of physiology2012
Oestrogen upregulates L-type Ca²⁺ channels via oestrogen-receptor- by a regional genomic mechanism in female rabbit hearts.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 70 citations in OpenAlex.
- Healthy human induced pluripotent stem cell-derived cardiomyocytes exhibit sex dimorphism even without the addition of hormones.Stem cells (Dayton, Ohio) · 2025Article
- Sex differences in cardiac dynamics during myocardial ischemia using a single cell approach.Scientific reports · 2025Article
- An In Vivo Model of Estrogen Supplementation Concerning the Expression of CaJournal of cardiovascular development and disease · 2024Article
- Moderate Endurance Exercise Increases Arrhythmia Susceptibility and Modulates Cardiac Structure and Function in a Sexually Dimorphic Manner.Journal of the American Heart Association · 2024Article
- Cardiac Injury After Traumatic Brain Injury: Clinical Consequences and Management.Neurocritical care · 2024Article
- Identifying sex similarities and differences in structure and function of the sinoatrial node in the mouse heart.Frontiers in medicine · 2024Article
- Rapid Pacing Decreases L-type CaThe Journal of membrane biology · 2023Article
- Review
- Higher NaInternational journal of molecular sciences · 2022Article
- Cardiovascular, Metabolic and Inflammatory Changes after Ovariectomy and Estradiol Substitution in Hereditary Hypertriglyceridemic Rats.International journal of molecular sciences · 2022Article
- GPER limits adverse changes to CaFrontiers in physiology · 2022Article
- A framework for developing sex-specific engineered heart models.Nature reviews. Materials · 2022Review
- Arrhythmic risk during pregnancy and postpartum in patients with long QT syndrome.Herzschrittmachertherapie & Elektrophysiologie · 2021Review
- TdP Incidence in Methoxamine-Sensitized Rabbit Model Is Reduced With Age but Not Influenced by Hypercholesterolemia.Frontiers in physiology · 2021Article
- Signalling mechanisms in the cardiovascular protective effects of estrogen: With a focus on rapid/membrane signalling.Current research in physiology · 2021Review
- The Link Between Sex Hormones and Susceptibility to Cardiac Arrhythmias: From Molecular Basis to Clinical Implications.Frontiers in cardiovascular medicine · 2021Review
- Pregnancy and oestrogen regulate sinoatrial node calcium homeostasis and accelerate pacemaking.Cardiovascular research · 2018Article
- Molecular pathways of oestrogen receptors and β-adrenergic receptors in cardiac cells: Recognition of their similarities, interactions and therapeutic value.Acta physiologica (Oxford, England) · 2018Review
- Calcium in Brugada Syndrome: Questions for Future Research.Frontiers in physiology · 2018Review
- Genomic upregulation of cardiac Cav1.2α and NCX1 by estrogen in women.Biology of sex differences · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
In type-2 long QT (LQT2), adult women and adolescent boys have a higher risk of lethal arrhythmias, called Torsades de pointes (TdP), compared to the opposite sex. In rabbit hearts, similar sex- and age-dependent TdP risks were attributed to higher expression levels of L-type Ca(2+) channels and Na(+)-Ca(2+) exchanger, at the base of the female epicardium. Here, the effects of oestrogen and progesterone are investigated to elucidate the mechanisms whereby I(Ca,L) density is upregulated in adult female rabbit hearts. I(Ca,L) density was measured by the whole-cell patch-clamp technique on days 0-3 in cardiomyocytes isolated from the base and apex of adult female epicardium. Peak I(Ca,L) was 28% higher at the base than apex (P < 0.01) and decreased gradually (days 0-3), becoming similar to apex myocytes, which had stable currents for 3 days. Incubation with oestrogen (E2, 0.1-1.0 nm) increased I(Ca,L) (∼2-fold) in female base but not endo-, apex or male myocytes. Progesterone (0.1-10 μm) had no effect at base myocytes. An agonist of the α- (PPT, 5 nm) but not the β- (DPN, 5 nm) subtype oestrogen receptor (ERα/ERβ) upregulated I(Ca,L) like E2. Western blots detected similar levels of ERα and ERβ in male and female hearts at the base and apex. E2 increased Cav1.2α (immunocytochemistry) and mRNA (RT-PCR) levels but did not change I(Ca,L) kinetics. I(Ca,L) upregulation by E2 was suppressed by the ER antagonist ICI 182,780 (10 μm) or by inhibition of transcription (actinomycin D, 4 μm) or protein biosynthesis (cycloheximide, 70 μm). Therefore, E2 upregulates I(Ca,L) by a regional genomic mechanism involving ERα which is a known determinant of sex differences in TdP risk in LQT2.
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Registered trials
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