A mechanosensitive cation channel in endothelial cells

Xiaoqiang Yao; H. Y. Kwan; Yu Huang

doi:10.1111/j.1540-8191.2001.tb01154.x

A mechanosensitive cation channel in endothelial cells

Xiaoqiang Yao, H. Y. Kwan, Yu Huang

Research output: Journal Publications and Reviews › RGC 21 - Publication in refereed journal › peer-review

9 Citations (Scopus)

Abstract

A mechanosensitive Ca2+-permeable channel is present in vascular endothelial cells. The activity of this channel increases in response to hemodynamic blood flow. Recently, it has been found that the activity of this channel may be regulated by cGMP through a protein kinase G-dependent pathway. Inhibition of the channel by cGMP abolishes the Ca2+ influx elicited by flow. Several inhibitors of the cation channel including Gd3+, Ni2+, and SK&F-96365 also inhibit the Ca2+ influx due to flow stimulation. These data suggest that a mechanosensitive cation channel is the primary pathway mediating the flow-induced Ca2+ entry in vascular endothelial cells.

Original language	English
Pages (from-to)	340-341
Journal	Journal of Cardiac Surgery
Volume	17
Issue number	4
DOIs	https://doi.org/10.1111/j.1540-8191.2001.tb01154.x
Publication status	Published - 1 Jul 2001
Externally published	Yes

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Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].

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abstract = "A mechanosensitive Ca2+-permeable channel is present in vascular endothelial cells. The activity of this channel increases in response to hemodynamic blood flow. Recently, it has been found that the activity of this channel may be regulated by cGMP through a protein kinase G-dependent pathway. Inhibition of the channel by cGMP abolishes the Ca2+ influx elicited by flow. Several inhibitors of the cation channel including Gd3+, Ni2+, and SK&F-96365 also inhibit the Ca2+ influx due to flow stimulation. These data suggest that a mechanosensitive cation channel is the primary pathway mediating the flow-induced Ca2+ entry in vascular endothelial cells.",

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AU - Yao, Xiaoqiang

AU - Kwan, H. Y.

AU - Huang, Yu

N1 - Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].

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N2 - A mechanosensitive Ca2+-permeable channel is present in vascular endothelial cells. The activity of this channel increases in response to hemodynamic blood flow. Recently, it has been found that the activity of this channel may be regulated by cGMP through a protein kinase G-dependent pathway. Inhibition of the channel by cGMP abolishes the Ca2+ influx elicited by flow. Several inhibitors of the cation channel including Gd3+, Ni2+, and SK&F-96365 also inhibit the Ca2+ influx due to flow stimulation. These data suggest that a mechanosensitive cation channel is the primary pathway mediating the flow-induced Ca2+ entry in vascular endothelial cells.

AB - A mechanosensitive Ca2+-permeable channel is present in vascular endothelial cells. The activity of this channel increases in response to hemodynamic blood flow. Recently, it has been found that the activity of this channel may be regulated by cGMP through a protein kinase G-dependent pathway. Inhibition of the channel by cGMP abolishes the Ca2+ influx elicited by flow. Several inhibitors of the cation channel including Gd3+, Ni2+, and SK&F-96365 also inhibit the Ca2+ influx due to flow stimulation. These data suggest that a mechanosensitive cation channel is the primary pathway mediating the flow-induced Ca2+ entry in vascular endothelial cells.

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M3 - RGC 21 - Publication in refereed journal

C2 - 12546083

SN - 0886-0440

VL - 17

SP - 340

EP - 341

JO - Journal of Cardiac Surgery

JF - Journal of Cardiac Surgery

IS - 4

ER -

A mechanosensitive cation channel in endothelial cells

Abstract

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