ArticleJournal of cellular physiology2010
Agonist-evoked Ca(2+) wave progression requires Ca(2+) and IP(3).
Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles.Advances in drug and alcohol research · 2021Article
- The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.Comprehensive Physiology · 2021Article
- Carbenoxolone and 18β-glycyrrhetinic acid inhibit inositol 1,4,5-trisphosphate-mediated endothelial cell calcium signalling and depolarise mitochondria.British journal of pharmacology · 2021Article
- Mechanisms underlying selective coupling of endothelial CaThe Journal of physiology · 2020Article
- FK506 regulates CaBritish journal of pharmacology · 2020Article
- Hydrogen peroxide depolarizes mitochondria and inhibits IPCell calcium · 2019Article
- Increased Vascular Contractility in Hypertension Results From Impaired Endothelial Calcium Signaling.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Calcium signals that determine vascular resistance.Wiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Endothelial TRPV4 channels modulate vascular tone by CaBritish journal of pharmacology · 2019Article
- CaThe Journal of physiology · 2019Article
- Mitochondrial ATP production provides long-range control of endothelial inositol trisphosphate-evoked calcium signaling.The Journal of biological chemistry · 2019Article
- Spatially structured cell populations process multiple sensory signals in parallel in intact vascular endothelium.Science signaling · 2018Article
- The Endothelium Solves Problems That Endothelial Cells Do Not Know Exist.Trends in pharmacological sciences · 2017Review
- Acetylcholine released by endothelial cells facilitates flow-mediated dilatation.The Journal of physiology · 2016Article
- Clusters of specialized detector cells provide sensitive and high fidelity receptor signaling in the intact endothelium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Pressure-dependent regulation of Ca2+ signalling in the vascular endothelium.The Journal of physiology · 2015Article
- Examining the role of mitochondria in Ca²⁺ signaling in native vascular smooth muscle.Microcirculation (New York, N.Y. : 1994) · 2013Review
- Pan-junctional sarcoplasmic reticulum in vascular smooth muscle: nanospace Ca2+ transport for site- and function-specific Ca2+ signalling.The Journal of physiology · 2013Review
- Article
- Microdomains of muscarinic acetylcholine and Ins(1,4,5)P₃ receptors create 'Ins(1,4,5)P₃ junctions' and sites of Ca²+ wave initiation in smooth muscle.Journal of cell science · 2012Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Smooth muscle responds to IP(3)-generating agonists by producing Ca(2+) waves. Here, the mechanism of wave progression has been investigated in voltage-clamped single smooth muscle cells using localized photolysis of caged IP(3) and the caged Ca(2+) buffer diazo-2. Waves, evoked by the IP(3)-generating agonist carbachol (CCh), initiated as a uniform rise in cytoplasmic Ca(2+) concentration ([Ca(2+)](c)) over a single though substantial length (approximately 30 microm) of the cell. During regenerative propagation, the wave-front was about 1/3 the length (approximately 9 microm) of the initiation site. The wave-front progressed at a relatively constant velocity although amplitude varied through the cell; differences in sensitivity to IP(3) may explain the amplitude changes. Ca(2+) was required for IP(3)-mediated wave progression to occur. Increasing the Ca(2+) buffer capacity in a small (2 microm) region immediately in front of a CCh-evoked Ca(2+) wave halted progression at the site. However, the wave front does not progress by Ca(2+)-dependent positive feedback alone. In support, colliding [Ca(2+)](c) increases from locally released IP(3) did not annihilate but approximately doubled in amplitude. This result suggests that local IP(3)-evoked [Ca(2+)](c) increases diffused passively. Failure of local increases in IP(3) to evoke waves appears to arise from the restricted nature of the IP(3) increase. When IP(3) was elevated throughout the cell, a localized increase in Ca(2+) now propagated as a wave. Together, these results suggest that waves initiate over a surprisingly large length of the cell and that both IP(3) and Ca(2+) are required for active propagation of the wave front to occur.
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