ArticleThe Journal of physiology2016
Acetylcholine released by endothelial cells facilitates flow-mediated dilatation.
Article in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
75 citing papers in PubMed, 121 citations in OpenAlex.
- Respiratory muscle training positively affects vasomotor response in young healthy women.PloS one · 2018Trial
- Klebsiella pneumoniae inhibits vasodilation through capsule and T6SS-dependent pathways.Nature microbiology · 2026Article
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- The Emerging Role of Endothelial Ion Channels in the Control of Human Microcirculation.International journal of molecular sciences · 2026Review
- Influence of the Cholinergic System on the Pathogenesis of Glioblastoma: Impact of the Neutrophil Granulocytes.International journal of molecular sciences · 2025Article
- Endothelial Cell Organization Drives Distinct Agonist-Specific CaActa physiologica (Oxford, England) · 2025Article
- The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- The machinery of healthy vasodilatation: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- Inside-Out IPFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Endogenous muscarinic acetylcholine receptor signaling blunts αAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Differential Gene and Protein Expressions Responsible for Vasomotor Signaling Provide Mechanistic Bases for the Opposite Flow-Induced Responses of Pre- and Post-Circle of Willis Arteries.Life (Basel, Switzerland) · 2025Article
- Mitochondria regulate inositol triphosphate-mediated CaThe Journal of physiology · 2025Article
- Long COVID - a critical disruption of cholinergic neurotransmission?Bioelectronic medicine · 2025Review
- Increased TRPV4 Channel Expression Enhances and Impairs Blood Vessel Function in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Flow-Dependent Modulation of Endothelial CaBiomedicines · 2024Article
- Endoplasmic Reticulum Stress Induces Vasodilation in Liver Vessels That Is Not Mediated by Unfolded Protein Response.International journal of molecular sciences · 2024Article
- Distinct neurochemical influences on fMRI response polarity in the striatum.Nature communications · 2024Article
- Muscarinic control of cardiovascular function in humans: a review of current clinical evidence.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2024Review
- Mini Review: the non-neuronal cardiac cholinergic system in type-2 diabetes mellitus.Frontiers in cardiovascular medicine · 2024Review
- Modelling hemodynamics regulation in rats and dogs to facilitate drugs safety risk assessment.Frontiers in pharmacology · 2024Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
key pointsThe endothelium plays a pivotal role in the vascular response to chemical and mechanical stimuli. The endothelium is exquisitely sensitive to ACh, although the physiological significance of ACh-induced activation of the endothelium is unknown. In the present study, we investigated the mechanisms of flow-mediated endothelial calcium signalling. Our data establish that flow-mediated endothelial calcium responses arise from the autocrine action of non-neuronal ACh released by the endothelium. ABSTRACT: Circulating blood generates frictional forces (shear stress) on the walls of blood vessels. These frictional forces critically regulate vascular function. The endothelium senses these frictional forces and, in response, releases various vasodilators that relax smooth muscle cells in a process termed flow-mediated dilatation. Although some elements of the signalling mechanisms have been identified, precisely how flow is sensed and transduced to cause the release of relaxing factors is poorly understood. By imaging signalling in large areas of the endothelium of intact arteries, we show that the endothelium responds to flow by releasing ACh. Once liberated, ACh acts to trigger calcium release from the internal store in endothelial cells, nitric oxide production and artery relaxation. Flow-activated release of ACh from the endothelium is non-vesicular and occurs via organic cation transporters. ACh is generated following mitochondrial production of acetylCoA. Thus, we show ACh is an autocrine signalling molecule released from endothelial cells, and identify a new role for the classical neurotransmitter in endothelial mechanotransduction.
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Registered trials
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.