ArticleThe Journal of physiology1999
Endothelium-dependent hyperpolarization and intercellular electrical coupling in guinea-pig mesenteric arterioles.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 197 citations in OpenAlex.
- Systems biology analysis of vasodynamics in mouse cerebral arterioles during resting state and functional hyperemia.PLoS computational biology · 2026Article
- Effects of SGLT2 inhibitors on ion channels in heart failure: focus on the endothelium.Basic research in cardiology · 2025Review
- CaInternational journal of molecular sciences · 2024Review
- Mechanosensing by Vascular Endothelium.Annual review of physiology · 2024Review
- Electro-metabolic signaling.The Journal of general physiology · 2024Article
- Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024Review
- The conducted vasomotor response and the principles of electrical communication in resistance arteries.Physiological reviews · 2024Review
- The capillary Kir channel as sensor and amplifier of neuronal signals: Modeling insights on KProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Calcium signals that determine vascular resistance.Wiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels.International journal of molecular sciences · 2018Review
- Piezo1 channels sense whole body physical activity to reset cardiovascular homeostasis and enhance performance.Nature communications · 2017Article
- Conducted dilatation to ATP and KActa physiologica (Oxford, England) · 2017Article
- Contribution of K(+) channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro.Pflugers Archiv : European journal of physiology · 2016Article
- Inward rectifier potassium (Kir2.1) channels as end-stage boosters of endothelium-dependent vasodilators.The Journal of physiology · 2016Article
- Ion channel networks in the control of cerebral blood flow.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Review
- Role of connexins and pannexins in cardiovascular physiology.Cellular and molecular life sciences : CMLS · 2015Review
- Eugenol dilates mesenteric arteries and reduces systemic BP by activating endothelial cell TRPV4 channels.British journal of pharmacology · 2015Article
- 5-hydroxytryptamine has an endothelium-derived hyperpolarizing factor-like effect on coronary flow in isolated rat hearts.Journal of biomedical science · 2015Article
- Vascular TRP channels: performing under pressure and going with the flow.Physiology (Bethesda, Md.) · 2014Review
- Syncytial communication in descending vasa recta includes myoendothelial coupling.American journal of physiology. Renal physiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Using the conventional whole-cell clamp method, the electrical responses of individual smooth muscle and endothelial cells to acetylcholine (ACh) were observed in multicellular preparations where the two types of cells remained in close apposition. 2. In both types of cells, ACh induced similar hyperpolarizing responses which, when recorded in current clamp mode, had two phases (an initial fast and a second slower phase). 3. After blocking gap junctions, including myoendothelial junctions, with 18beta-glycyrrhetinic acid, ACh induced an outward current with two phases in voltage-clamped endothelial cells. The outward current appeared around -90 mV and increased linearly with the membrane depolarization. 4. In smooth muscle cells, ACh failed to induce a membrane current after gap junctions had been blocked with 18beta-glycyrrhetinic acid. The inhibition of ACh-induced response by 18beta-glycyrrhetinic acid was observed using either sharp or patch electrodes. 5. Nominally Ca2+-free solution reduced the initial phase and abolished the second phase of ACh-induced responses of endothelial cells. Both phases were also reduced by charybdotoxin (CTX). 6. Our results indicate that in guinea-pig mesenteric arterioles, ACh hyperpolarizes endothelial cells by activating Ca2+-activated K+ channels which are sensitive to CTX. On the other hand, hyperpolarizing responses detected in smooth muscle cells seem to originate in endothelial cells and conduct to the muscle layer via myoendothelial gap junctions.
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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.