ArticleThe Journal of physiology2003
Synergism between inositol phosphates and diacylglycerol on native TRPC6-like channels in rabbit portal vein myocytes.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Transient receptor potential channel-dependent myogenic responsiveness in small-sized resistance arteries.Journal of exercise rehabilitation · 2021Review
- PIPProceedings of the National Academy of Sciences of the United States of America · 2020Review
- TRPC channels: Structure, function, regulation and recent advances in small molecular probes.Pharmacology & therapeutics · 2020Review
- Regulation of Membrane Calcium Transport Proteins by the Surrounding Lipid Environment.Biomolecules · 2019Review
- Calcium signals that determine vascular resistance.Wiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- A Closely Associated Phospholipase C Regulates Cation Channel Function through Phosphoinositide Hydrolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Dual action of the GαScientific reports · 2018Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology.Antioxidants & redox signaling · 2016Review
- Diacylglycerol-mediated regulation of Aplysia bag cell neuron excitability requires protein kinase C.The Journal of physiology · 2016Article
- Inositol 1,4,5-trisphosphate activates TRPC3 channels to cause extracellular Ca2+ influx in airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Divergent signaling mechanisms for venous versus arterial contraction as revealed by endothelin-1.Journal of vascular surgery · 2015Article
- Transient receptor potential channels in the vasculature.Physiological reviews · 2015Review
- TRPC6 inhibited NMDA current in cultured hippocampal neurons.Neuromolecular medicine · 2013Article
- Inositol trisphosphate receptors in smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2012Review
- Integration of transient receptor potential canonical channels with lipids.Acta physiologica (Oxford, England) · 2012Review
- TRPC channels in smooth muscle cells.Frontiers in bioscience (Landmark edition) · 2010Review
- Ins(1,4,5)P3 interacts with PIP2 to regulate activation of TRPC6/C7 channels by diacylglycerol in native vascular myocytes.The Journal of physiology · 2010Article
- Activation of native TRPC1/C5/C6 channels by endothelin-1 is mediated by both PIP3 and PIP2 in rabbit coronary artery myocytes.The Journal of physiology · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In rabbit portal vein myocytes noradrenaline activates a non-selective cation current (Icat) which involves a transient receptor potential protein (TRPC6). Previously we have shown that the diaylglycerol (DAG) analogue 1-oleoyl-2-acetyl-sn-glycerol (OAG) stimulates Icat via a protein kinase C (PKC)-independent mechanism, and in the present study we have investigated the interaction between inositol phosphates (InsPs) and OAG on Icat. With whole-cell recording of Icat from freshly isolated rabbit portal vein myocytes the amplitude and rate of activation of noradrenaline-evoked Icat were much greater than those of OAG-induced Icat. Inclusion of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) in the pipette solution did not evoke Icat but greatly potentiated the amplitude and rate of activation of OAG-induced Icat. With isolated outside-out patches Ins(1,4,5)P3 markedly increased the rate of activation and the open probability of OAG-evoked channel activity, with no change in unitary conductance, channel mean open times or burst durations. The effects of Ins(1,4,5)P3 were mimicked by Ins(2,4,5)P3, 3-F-Ins(1,4,5)P3 and Ins(1,4)P2 but not by Ins(1,3,4,5)P4 and the potentiating effects of InsPs were not inhibited by heparin. Therefore it is concluded that both DAG and InsPs are necessary for full activation of Icat by noradrenaline and the effect of InsPs is via a heparin-insensitive mechanism and represents a novel action of InsPs.
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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.