scholarly journals Mutual Antagonism of Calcium Entry by Capacitative and Arachidonic Acid-mediated Calcium Entry Pathways

2001 ◽  
Vol 276 (23) ◽  
pp. 20186-20189 ◽  
Author(s):  
Dali Luo ◽  
Lisa M. Broad ◽  
Gary St. J. Bird ◽  
James W. Putney
Keyword(s):  
Arachidonic Acid ◽  
Calcium Entry ◽  
Mutual Antagonism

ARC Channels: A Novel Pathway for Receptor-Activated Calcium Entry

Physiology ◽  
2004 ◽  
Vol 19 (6) ◽  
pp. 355-361 ◽  
Author(s):  
Trevor J. Shuttleworth ◽  
Jill L. Thompson ◽  
Olivier Mignen
Keyword(s):  
Arachidonic Acid ◽  
Calcium Entry ◽  
Reciprocal Regulation ◽  
Functional Implications

In many nonexcitable cells, stimulation with low agonist concentrations specifically activates Ca2+ entry via arachidonic acid-regulated, highly Ca2+-selective ARC channels. Only at high agonist concentrations are the more widely studied store-operated channels activated, producing sustained elevated cytosolic Ca2+ concentration signals. These signals activate calcineurin, which in turn inhibits the ARC channels, resulting in a “reciprocal regulation” of these two distinct Ca2+-entry pathways that may have important functional implications for the cell.

Calcium entry and the control of calcium oscillations

2003 ◽  
Vol 31 (5) ◽  
pp. 916-919 ◽  
Author(s):  
T.J. Shuttleworth ◽  
O. Mignen
Keyword(s):  
Arachidonic Acid ◽  
Critical Role ◽  
Cell Types ◽  
Calcium Entry ◽  
Calcium Oscillations ◽  
Reciprocal Regulation ◽  
Crac Channels ◽  
Store Depletion ◽  
Low Concentrations ◽  
Ca2 Channels

During oscillatory Ca2+ signals, the agonist-induced enhanced entry of extracellular Ca2+ plays a critical role in modulating the frequency of the oscillations. Although it was originally assumed that the entry of Ca2+ under these conditions occurred via the well-known, and apparently ubiquitous, store-operated mechanism, subsequent studies suggested that this was unlikely. It is now known that, in many cell types, a novel non-capacitative Ca2+-selective pathway whose activation is dependent on arachidonic acid is responsible, and the channels involved [ARC channels (arachidonate-regulated Ca2+ channels)] have been characterized. These ARC channels co-exist with the store-operated CRAC channels (Ca2+-release-activated Ca2+ channel) in cells, but each plays a unique and non-overlapping role in Ca2+ signalling. In particular, it is the ARC channels that are specifically activated at the low agonist concentrations that give rise to oscillatory Ca2+ signals and provide the predominant mode of Ca2+ entry under these conditions. The indications are that Ca2+ entry through the ARC channels increases the likelihood that low concentrations of Ins(1,4,5)P3 will trigger repetitive Ca2+ release. At higher agonist concentrations, store-depletion is more complete and sustained resulting in the activation of CRAC channels. At the same time the ARC channels are turned off, resulting in what we have described as a reciprocal regulation of these two distinct Ca2+ entry pathways.

Regulation of noncapacitative calcium entry by arachidonic acid and nitric oxide in endothelial cells

2005 ◽  
Vol 19 (14) ◽  
pp. 2075-2077 ◽  
Author(s):  
Annalisa Mottola ◽  
Susanna Antoniotti ◽  
Davide Lovisolo ◽  
Luca Munaron
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Calcium Entry

Arachidonic acid mediates non-capacitative calcium entry evoked by CB1-cannabinoid receptor activation in DDT1 MF-2 smooth muscle cells

2005 ◽  
Vol 205 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Dirk G. Demuth ◽  
Effimia Gkoumassi ◽  
Melloney J. Dröge ◽  
Bart G.J. Dekkers ◽  
Henk J. Esselink ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cannabinoid Receptor ◽  
Muscle Cells ◽  
Receptor Activation ◽  
Calcium Entry ◽  
Capacitative Calcium Entry ◽  
Cb1 Cannabinoid Receptor

TRPV4 initiates the acute calcium-dependent permeability increase during ventilator-induced lung injury in isolated mouse lungs

2007 ◽  
Vol 293 (4) ◽  
pp. L923-L932 ◽  
Author(s):  
Kazutoshi Hamanaka ◽  
Ming-Yuan Jian ◽  
David S. Weber ◽  
Diego F. Alvarez ◽  
Mary I. Townsley ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Vascular Permeability ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Ruthenium Red ◽  
Calcium Entry ◽  
Transient Receptor Potential Vanilloid ◽  
Pulmonary Vascular Permeability ◽  
Permeability Increase ◽  
Mouse Lungs

We have previously implicated calcium entry through stretch-activated cation channels in initiating the acute pulmonary vascular permeability increase in response to high peak inflation pressure (PIP) ventilation. However, the molecular identity of the channel is not known. We hypothesized that the transient receptor potential vanilloid-4 (TRPV4) channel may initiate this acute permeability increase because endothelial calcium entry through TRPV4 channels occurs in response to hypotonic mechanical stress, heat, and P-450 epoxygenase metabolites of arachidonic acid. Therefore, permeability was assessed by measuring the filtration coefficient (Kf) in isolated perfused lungs of C57BL/6 mice after 30-min ventilation periods of 9, 25, and 35 cmH2O PIP at both 35°C and 40°C. Ventilation with 35 cmH2O PIP increased Kf by 2.2-fold at 35°C and 3.3-fold at 40°C compared with baseline, but Kf increased significantly with time at 40°C with 9 cmH2O PIP. Pretreatment with inhibitors of TRPV4 (ruthenium red), arachidonic acid production (methanandamide), or P-450 epoxygenases (miconazole) prevented the increases in Kf. In TRPV4−/− knockout mice, the high PIP ventilation protocol did not increase Kf at either temperature. We have also found that lung distention caused Ca2+ entry in isolated mouse lungs, as measured by ratiometric fluorescence microscopy, which was absent in TRPV4−/− and ruthenium red-treated lungs. Alveolar and perivascular edema was significantly reduced in TRPV4−/− lungs. We conclude that rapid calcium entry through TRPV4 channels is a major determinant of the acute vascular permeability increase in lungs following high PIP ventilation.

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