ArticleThe Journal of physiology2019
Oxytocin can regulate myometrial smooth muscle excitability by inhibiting the Na
Article in The Journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Ion Channels as Gatekeepers of Fertility: from Uterine Kir7.1 to Sperm CatSper.Physiology (Bethesda, Md.) · 2027Review
- Myometrial mechanotransduction and the timing of parturition: ion-channel pathways linking uterine stretch, calcium signaling, and inflammation.Frontiers in physiology · 2026Review
- Fluorescent Peptide Tracers for Simultaneous Oxytocin Receptor Activation and Visualization.Angewandte Chemie (International ed. in English) · 2025Article
- SLO2.1/NALCN Functional Complex Activity in Mouse Myometrial Smooth Muscle Cells During Pregnancy.Journal of cellular physiology · 2025Article
- The extracellular vesicles of boar seminal plasma contain oxytocin at levels associated with fertility.Extracellular vesicles and circulating nucleic acids · 2025Article
- Review
- Review
- Arrest of mouse preterm labor until term delivery by combination therapy with atosiban and mundulone, a natural product with tocolytic efficacy.Pharmacological research · 2023Article
- SLO3: A Conserved Regulator of Sperm Membrane Potential.International journal of molecular sciences · 2023Review
- The mechanism of oxytocin and its receptors in regulating cells in bone metabolism.Frontiers in pharmacology · 2023Review
- Mechanism and Pharmacodynamic Substance Basis of Raw and Wine-ProcessedPain research & management · 2023Article
- Mechanism of Oxytocin-Induced Contraction in Rat Gastric Circular Smooth Muscle.International journal of molecular sciences · 2022Article
- Perinatal outcome and risk factors of precipitate labor in term primipara: an analysis of 381 cases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Article
- Oxytocin: A Multi-Functional Biomolecule with Potential Actions in Dysfunctional Conditions; From Animal Studies and Beyond.Biomolecules · 2022Review
- Modeling and experimental approaches for elucidating multi-scale uterine smooth muscle electro- and mechano-physiology: A review.Frontiers in physiology · 2022Review
- Oxytocin in Women's Health and Disease.Frontiers in endocrinology · 2022Review
- Article
- Uterine contractions in rodent models and humans.Acta physiologica (Oxford, England) · 2021Review
- Progesterone receptor isoform B regulates theProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Relaxant Effects of the Aqueous Extract ofBioMed research international · 2021Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
key pointsAt the end of pregnancy, the uterus transitions from a quiescent state to a highly contractile state. This transition requires that the uterine (myometrial) smooth muscle cells increase their excitability, although how this occurs is not fully understood. We identified SLO2.1, a potassium channel previously unknown in uterine smooth muscle, as a potential significant contributor to the electrical excitability of myometrial smooth muscle cells. We found that activity of the SLO2.1 channel is negatively regulated by oxytocin via Gαq-protein-coupled receptor activation of protein kinase C. This results in depolarization of the uterine smooth muscle cells and calcium entry, which may contribute to uterine contraction. These findings provide novel insights into a previously unknown mechanism by which oxytocin may act to modulate myometrial smooth muscle cell excitability. Our findings also reveal a new potential pharmacological target for modulating uterine excitability. ABSTRACT: During pregnancy, the uterus transitions from a quiescent state to a more excitable contractile state. This is considered to be at least partly a result of changes in the myometrial smooth muscle cell (MSMC) resting membrane potential. However, the ion channels controlling the myometrial resting membrane potential and the mechanism of transition to a more excitable state have not been fully clarified. In the present study, we show that the sodium-activated, high-conductance, potassium leak channel, SLO2.1, is expressed and active at the resting membrane potential in MSMCs. Additionally, we report that SLO2.1 is inhibited by oxytocin binding to the oxytocin receptor. Inhibition of SLO2.1 leads to membrane depolarization and activation of voltage-dependent calcium channels, resulting in calcium influx. The results of the present study reveal that oxytocin may modulate MSMC electrical activity by inhibiting SLO2.1 potassium channels.
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