Acute modulation of Ca2+ influx on rat heart by 17β-estradiol
Abstract
Estrogens initiate their action by binding to specific intracellular receptors and then acting on gene expression. In addition, there is growing evidence of a direct membrane effect via interaction with a cell surphase receptor. The aim of the present study was to investigate the acute effects of 17beta-estradiol on Ca2+ fluxes through second messenger pathways in rat cardiac muscle. Exposure of rat ventricle to low levels of 17beta-estradiol (10(-12)-10(-8) M) increased 45Ca2+ influx within 1 min (+38%); the response was biphasic, peaking at 2 and 5 min (+60 and +55%, respectively). The effect of the hormone on rat heart seems to be specific since 17alpha-estradiol, dihydrotestosterone, and progesterone were devoid of activity. The effect of 17beta-estradiol (5 min, 10(-10) M) was suppressed by nitrendipine (1 microM) and LaCl3 (10 microM), involving the activation of voltage-dependent Ca2+ channels in the acute increase of rat heart calcium influx by the hormone. 17Beta-estradiol rapidly increased cAMP content and PKA activity of rat cardiac muscle in parallel to the changes in Ca2+ uptake. In addition the cAMP antagonist Rp-cAMPS suppressed 17beta-estradiol-dependent Ca2+ influx. Altogether, the data suggest the involvement of the cAMP/PKA messenger system in the nongenomic modulation of Ca2+ influx in rat cardiac muscle by physiological levels of 17beta-estradiol.
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The bulk of studies evaluating sex differences in the AF-related risk of heart failure have showed no significant difference; however, a few studies have suggested higher risk in women.
“The bulk of studies evaluating sex differences in the AF-related risk of HF have showed no significant difference; however, a few studies have suggested higher risk in women (Supplementary Table S8).”
From Atrial fibrillation in women: epidemiology, pathophysiology, presentation, and prognosis (2016) · cites this paper as [101]
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Atrial fibrillation in women: epidemiology, pathophysiology, presentation, and prognosis
Ko, D., Rahman, F., Schnabel, R. B., Yin, X., Benjamin, E. J., & Christophersen, I. E. (2016) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2016.45 · Cited by 353 · see citing works
- Authors
- Buitrago, C., Massheimer, V., & de Boland, A. R.
- Affiliations
- Universidad Nacional del Sur (AR)
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2000-01
- Volume
- 12
- Issue
- 1
- Pages
- 47-52
- ISSN
- 0898-6568 (ISSN-L)
- OpenAlex
- W2045363416
- Cited by
- 30
- References
- 43
- Citations by year
- 2026: 2 · 2024: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2018: 1 · 2016: 1 · 2015: 3 · 2012: 2
- FWCI
- 1.55
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cellular Signalling (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- estradiol, estrogen, calcium influx, myocardium, non-genomic estrogen signaling, voltage-gated calcium channels, cAMP/PKA signaling, second messenger pathways, membrane estrogen receptor, nitrendipine, lanthanum chloride, rat ventricle
- MeSH terms
- Animals, Calcium, Estradiol, Female, Myocardium, Signal Transduction, Ion Transport, Rats, Wistar, Rats, In Vitro Techniques
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