ArticleThe Journal of physiology2002
Discrete store-operated calcium influx into an intracellular compartment in rabbit arteriolar smooth muscle.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 61 citations in OpenAlex.
- A multiscale active structural model of the arterial wall accounting for smooth muscle dynamics.Journal of the Royal Society, Interface · 2018Article
- Hydrogen peroxide activates store-operated Ca(2+) entry in coronary arteries.British journal of pharmacology · 2015Article
- Altered reactivity of resistance vasculature contributes to hypertension in elastin insufficiency.American journal of physiology. Heart and circulatory physiology · 2014Article
- Cross talk between plasma membrane Na(+)/Ca (2+) exchanger-1 and TRPC/Orai-containing channels: key players in arterial hypertension.Advances in experimental medicine and biology · 2013Article
- Orai1 calcium channels in the vasculature.Pflugers Archiv : European journal of physiology · 2012Review
- Caveolin-1 assembles type 1 inositol 1,4,5-trisphosphate receptors and canonical transient receptor potential 3 channels into a functional signaling complex in arterial smooth muscle cells.The Journal of biological chemistry · 2011Article
- TRPC1 and STIM1 mediate capacitative Ca2+ entry in mouse pulmonary arterial smooth muscle cells.The Journal of physiology · 2009Article
- IP3 constricts cerebral arteries via IP3 receptor-mediated TRPC3 channel activation and independently of sarcoplasmic reticulum Ca2+ release.Circulation research · 2008Article
- Store-operated calcium entry in vascular smooth muscle.British journal of pharmacology · 2008Review
- High-resolution in vivo imaging of the neurovascular unit during spreading depression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Mechanisms of the prostaglandin F2alpha-induced rise in [Ca2+]i in rat intrapulmonary arteries.The Journal of physiology · 2006Article
- TRPC1: store-operated channel and more.Pflugers Archiv : European journal of physiology · 2005Review
- Emerging functions of 10 types of TRP cationic channel in vascular smooth muscle.Clinical and experimental pharmacology & physiology · 2005Review
- Visualization of localized store-operated calcium entry in mouse astrocytes. Close proximity to the endoplasmic reticulum.The Journal of physiology · 2005Article
- Membrane hyperpolarization is not required for sustained muscarinic agonist-induced increases in intracellular Ca2+ in arteriolar endothelial cells.Microcirculation (New York, N.Y. : 1994) · 2005Article
- Non-selective cationic channels of smooth muscle and the mammalian homologues of Drosophila TRP.The Journal of physiology · 2004Review
- Gadolinium reduces short-term stretch-induced muscle damage in isolated mdx mouse muscle fibres.The Journal of physiology · 2003Article
- Capacitative calcium entry as a pulmonary specific vasoconstrictor mechanism in small muscular arteries of the rat.British journal of pharmacology · 2003Article
- Pharmacological profile of store-operated channels in cerebral arteriolar smooth muscle cells.British journal of pharmacology · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study tested the hypothesis that store-operated channels (SOCs) exist as a discrete population of Ca2+ channels activated by depletion of intracellular Ca(2+) stores in cerebral arteriolar smooth muscle cells and explored their direct contractile function. Using the Ca2+ indicator fura-PE3 it was observed that depletion of sarcoplasmic reticulum (SR) Ca2+ by inhibition of SR Ca2+-ATPase (SERCA) led to sustained elevation of [Ca2+]i that depended on extracellular Ca2+ and slightly enhanced Mn2+ entry. Enhanced background Ca2+ influx did not explain the raised [Ca2+]i in response to SERCA inhibitors because it had marked gadolinium (Gd3+) sensitivity, which background pathways did not. Effects were not secondary to changes in membrane potential. Thus SR Ca2+ depletion activated SOCs. Strikingly, SOC-mediated Ca2+ influx did not evoke constriction of the arterioles, which were in a resting state. This was despite the fura-PE3-indicated [Ca2+]i rise being greater than that evoked by 20 mM [K+]o (which did cause constriction). Release of endothelial vasodilators did not explain the absence of SOC-mediated constriction, nor did a change in Ca2+ sensitivity of the contractile proteins. We suggest SOCs are a discrete subset of Ca2+ channels allowing Ca2+ influx into a 'non-contractile' compartment in cerebral arteriolar smooth muscle cells.
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