ArticleAmerican journal of physiology. Cell physiology2010
Ca2+ release from the sarcoplasmic reticulum is required for sustained TRPM4 activity in cerebral artery smooth muscle cells.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 103 citations in OpenAlex.
- Ryanodine receptor cluster remodeling linksbioRxiv : the preprint server for biology · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- TRPM4 Couples Mechanical Force to Myogenic Constriction Throughout the Resistance Vasculature.bioRxiv : the preprint server for biology · 2026Article
- Pacemaking in the lymphatic system.The Journal of physiology · 2026Review
- Knockdown of FKBP12.6 may Cause Bladder Dysfunction in Mice by Affecting IP3R/TRPM4 Function.Current medicinal chemistry · 2026Article
- Unresolved mechanisms: a hypothesized spatial regulation of myosin light chain phosphorylation within the walls of resistance arteries.Frontiers in physiology · 2026Article
- Endothelial CYB5R3 couples store-operated calcium entry to TRPV2 activation and vascular fitness.bioRxiv : the preprint server for biology · 2025Article
- The TRP channels serving as chemical-to-electrical signal converter.Physiological reviews · 2025Review
- β-Adrenergic Blockers Increase cAMP and Stimulate Insulin Secretion Through a PKA/RYR2/TRPM5 Pathway in Pancreatic β-Cells In Vitro.Pharmacology research & perspectives · 2025Article
- Transient Receptor Potential Channels in Vascular Mechanotransduction.American journal of hypertension · 2025Review
- IP3R1 underlies diastolic ANO1 activation and pressure-dependent chronotropy in lymphatic collecting vessels.The Journal of general physiology · 2023Article
- Impaired intracellular CaScience signaling · 2023Article
- Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Endoplasmic Reticulum-Plasma Membrane Junctions as Sites of Depolarization-Induced CaAnnual review of physiology · 2023Review
- Faulty TRPM4 channels underlie age-dependent cerebral vascular dysfunction in Gould syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Differential effects of TRPM4 channel inhibitors on Guinea pig urinary bladder smooth muscle excitability and contractility: Novel 4-chloro-2-[2-(2-chloro-phenoxy)-acetylamino]-benzoic acid (CBA) versus classical 9-phenanthrol.Pharmacology research & perspectives · 2022Article
- Ischemic postconditioning reduces spinal cord ischemia-reperfusion injury through ATP-sensitive potassium channel.Spinal cord · 2022Article
- STIM1-dependent peripheral coupling governs the contractility of vascular smooth muscle cells.eLife · 2022Article
- Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 1: Modulation of TRPM4.Pharmaceuticals (Basel, Switzerland) · 2022Review
20 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The melastatin transient receptor potential (TRP) channel TRPM4 is a critical regulator of vascular smooth muscle cell membrane potential and contractility. Activation of the channel is Ca(2+)-dependent, but prolonged exposure to high (>1 microM) levels of intracellular Ca(2+) causes rapid (within approximately 2 min) desensitization of TRPM4 currents under conventional whole cell and inside-out patch-clamp conditions. The goal of the present study was to establish a novel method to record sustained TRPM4 currents in smooth muscle cells under near-physiological conditions. Using the amphotericin B-perforated patch-clamp technique, we recorded and characterized sustained (up to 30 min) transient inward cation currents (TICCs) in freshly isolated cerebral artery myocytes. In symmetrical cation solutions, TICCs reversed at 0 mV and had an apparent unitary conductance of 25 pS. Replacement of extracellular Na(+) with the nonpermeable cation N-methyl-d-glucamine abolished the current. TICC activity was attenuated by the TRPM4 blockers fluflenamic acid and 9-phenanthrol. Selective silencing of TRPM4 expression using small interfering RNA diminished TICC activity, suggesting that the molecular identity of the responsible ion channel is TRPM4. We used the perforated patch-clamp method to test the hypothesis that TRPM4 is activated by intracellular Ca(2+) signaling events. We found that TICC activity is independent of Ca(2+) influx and ryanodine receptor activity but is attenuated by sarco(endo)plasmic reticulum Ca(2+)-ATPase inhibition and blockade of inositol 1,4,5-trisphosphate receptor-mediated Ca(2+) release from the sarcoplasmic reticulum. Our findings suggest that TRPM4 channels in cerebral artery myocytes are regulated by Ca(2+) release from inositol 1,4,5-trisphosphate receptor on the sarcoplasmic reticulum.
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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.