ArticleThe Journal of physiology2015
Membrane potential governs calcium influx into microvascular endothelium: integral role for muscarinic receptor activation.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
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- Voltage-Dependent Ion Channels in Vascular Endothelial Cells: An Unexpected Signaling Pathway in Non-Excitable Cells.Biomedicines · 2026Review
- The Emerging Role of Endothelial Ion Channels in the Control of Human Microcirculation.International journal of molecular sciences · 2026Review
- Even breathing gets old: Impact of ageing on small arteries of the diaphragm.The Journal of physiology · 2025Article
- Mitochondrial Ca2+-coupled generation of reactive oxygen species, peroxynitrite formation, and endothelial dysfunction in Cantú syndrome.JCI insight · 2024Article
- The conducted vasomotor response and the principles of electrical communication in resistance arteries.Physiological reviews · 2024Review
- Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems.American journal of physiology. Heart and circulatory physiology · 2023Review
- Intraluminal pressure elevates intracellular calcium and contracts CNS pericytes: Role of voltage-dependent calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Gsmtx4 Alleviated Osteoarthritis through Piezo1/Calcineurin/NFAT1 Signaling Axis under Excessive Mechanical Strain.International journal of molecular sciences · 2023Article
- KMicrocirculation (New York, N.Y. : 1994) · 2023Article
- Potassium Channels in the Uterine Vasculature: Role in Healthy and Complicated Pregnancies.International journal of molecular sciences · 2022Review
- ATP and acetylcholine interact to modulate vascular tone and αJournal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- CaMolecular microbiology · 2021Article
- KCa channel activation normalizes endothelial function in Type 2 Diabetic resistance arteries by improving intracellular CaMetabolism: clinical and experimental · 2021Article
- Aging Alters Cerebrovascular Endothelial GPCR and K+ Channel Function: Divergent Role of Biological Sex.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
- Development of Alzheimer's Disease Progressively Alters Sex-Dependent KCa and Sex-Independent KIR Channel Function in Cerebrovascular Endothelium.Journal of Alzheimer's disease : JAD · 2020Article
- Functional Interaction among KInternational journal of molecular sciences · 2019Review
- Simultaneous Measurements of Intracellular Calcium and Membrane Potential in Freshly Isolated and Intact Mouse Cerebral Endothelium.Journal of visualized experiments : JoVE · 2019Article
- Internalization and Transportation of Endothelial Cell Surface KOxidative medicine and cellular longevity · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In resistance arteries, coupling a rise of intracellular calcium concentration ([Ca(2+)]i) to endothelial cell hyperpolarization underlies smooth muscle cell relaxation and vasodilatation, thereby increasing tissue blood flow and oxygen delivery. A controversy persists as to whether changes in membrane potential (V(m)) alter endothelial cell [Ca(2+)]i. We tested the hypothesis that V(m) governs [Ca(2+)]i in endothelium of resistance arteries by performing Fura-2 photometry while recording and controlling V(m) of intact endothelial tubes freshly isolated from superior epigastric arteries of C57BL/6 mice. Under resting conditions, [Ca(2+)]i did not change when V(m) shifted from baseline (∼-40 mV) via exposure to 10 μM NS309 (hyperpolarization to ∼-80 mV), via equilibration with 145 mm [K(+)]o (depolarization to ∼-5 mV), or during intracellular current injection (±0.5 to 5 nA, 20 s pulses) while V(m) changed linearly between ∼-80 mV and +10 mV. In contrast, during the plateau (i.e. Ca(2+) influx) phase of the [Ca(2+)]i response to approximately half-maximal stimulation with 100 nm ACh (∼EC50), [Ca(2+)]i increased as V(m) hyperpolarized below -40 mV and decreased as V(m) depolarized above -40 mV. The magnitude of [Ca(2+)]i reduction during depolarizing current injections correlated with the amplitude of the plateau [Ca(2+)]i response to ACh. The effect of hyperpolarization on [Ca(2+)]i was abolished following removal of extracellular Ca(2+), was enhanced subtly by raising extracellular [Ca(2+)] from 2 mm to 10 mm and was reduced by half in endothelium of TRPV4(-/-) mice. Thus, during submaximal activation of muscarinic receptors, V(m) can modulate Ca(2+) entry through the plasma membrane in accord with the electrochemical driving force.
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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.