Cyclic nucleotides and Ca2+ influx pathways in vascular endothelial cells

H. Y. Kwan; Y. Huang; X. Yao

Cyclic nucleotides and Ca²⁺ influx pathways in vascular endothelial cells

H. Y. Kwan
, Y. Huang
, X. Yao^*

^*Corresponding author for this work

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

10 Citations (Scopus)

Abstract

Ca²⁺ mobilizing agonists and hemodynamic shear stress both elicit a rise in endothelial cytosolic Ca²⁺ [Ca²⁺]_i, which then acts to stimulate nitric oxide synthase and phospholipase A₂, leading to the production and release of nitric oxide (NO) and other vascular substances such as prostacyclin and endothelium-derived hyperpolarizing factors (EDHF). In this article, regulatory mechanisms of agonist-induced and mechanosensitive Ca²⁺ influx pathways in vascular endothelial cells will be discussed. Special emphasis will be placed on the regulation of agonist-induced Ca²⁺ influx by protein kinase G (PKG). Flow-induced Ca²⁺ influx in relation to vascular dilation and the vasodilator produced will also be discussed. © 2007 - IOS Press and the authors. All rights reserved.

Original language	English
Pages (from-to)	63-70
Journal	Clinical Hemorheology and Microcirculation
Volume	37
Issue number	1-2
Publication status	Published - 2007
Externally published	Yes

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Kwan, H. Y., Huang, Y., & Yao, X. (2007). Cyclic nucleotides and Ca²⁺ influx pathways in vascular endothelial cells. Clinical Hemorheology and Microcirculation, 37(1-2), 63-70. https://journals.sagepub.com/doi/abs/10.3233/CHM-2007-1002?_gl=1*1lhibc9*_up*MQ..*_ga*MTEzMjIyMTMyNS4xNzcwOTQ1MDQ0*_ga_60R758KFDG*czE3NzA5NDUwNDQkbzEkZzEkdDE3NzA5NDUwODgkajE2JGwwJGg5NjQ5ODUxNTg.

@article{3f15a52d91cb45b1b9ba260b573faad9,

title = "Cyclic nucleotides and Ca2+ influx pathways in vascular endothelial cells",

abstract = "Ca2+ mobilizing agonists and hemodynamic shear stress both elicit a rise in endothelial cytosolic Ca2+ [Ca2+]i, which then acts to stimulate nitric oxide synthase and phospholipase A2, leading to the production and release of nitric oxide (NO) and other vascular substances such as prostacyclin and endothelium-derived hyperpolarizing factors (EDHF). In this article, regulatory mechanisms of agonist-induced and mechanosensitive Ca2+ influx pathways in vascular endothelial cells will be discussed. Special emphasis will be placed on the regulation of agonist-induced Ca2+ influx by protein kinase G (PKG). Flow-induced Ca2+ influx in relation to vascular dilation and the vasodilator produced will also be discussed. {\textcopyright} 2007 - IOS Press and the authors. All rights reserved.",

author = "Kwan, \{H. Y.\} and Y. Huang and X. Yao",

note = "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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journal = "Clinical Hemorheology and Microcirculation",

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Kwan, HY, Huang, Y & Yao, X 2007, 'Cyclic nucleotides and Ca²⁺ influx pathways in vascular endothelial cells', Clinical Hemorheology and Microcirculation, vol. 37, no. 1-2, pp. 63-70. <https://journals.sagepub.com/doi/abs/10.3233/CHM-2007-1002?_gl=1*1lhibc9*_up*MQ..*_ga*MTEzMjIyMTMyNS4xNzcwOTQ1MDQ0*_ga_60R758KFDG*czE3NzA5NDUwNDQkbzEkZzEkdDE3NzA5NDUwODgkajE2JGwwJGg5NjQ5ODUxNTg.>

TY - JOUR

T1 - Cyclic nucleotides and Ca2+ influx pathways in vascular endothelial cells

AU - Kwan, H. Y.

AU - Huang, Y.

AU - Yao, X.

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].

PY - 2007

Y1 - 2007

N2 - Ca2+ mobilizing agonists and hemodynamic shear stress both elicit a rise in endothelial cytosolic Ca2+ [Ca2+]i, which then acts to stimulate nitric oxide synthase and phospholipase A2, leading to the production and release of nitric oxide (NO) and other vascular substances such as prostacyclin and endothelium-derived hyperpolarizing factors (EDHF). In this article, regulatory mechanisms of agonist-induced and mechanosensitive Ca2+ influx pathways in vascular endothelial cells will be discussed. Special emphasis will be placed on the regulation of agonist-induced Ca2+ influx by protein kinase G (PKG). Flow-induced Ca2+ influx in relation to vascular dilation and the vasodilator produced will also be discussed. © 2007 - IOS Press and the authors. All rights reserved.

AB - Ca2+ mobilizing agonists and hemodynamic shear stress both elicit a rise in endothelial cytosolic Ca2+ [Ca2+]i, which then acts to stimulate nitric oxide synthase and phospholipase A2, leading to the production and release of nitric oxide (NO) and other vascular substances such as prostacyclin and endothelium-derived hyperpolarizing factors (EDHF). In this article, regulatory mechanisms of agonist-induced and mechanosensitive Ca2+ influx pathways in vascular endothelial cells will be discussed. Special emphasis will be placed on the regulation of agonist-induced Ca2+ influx by protein kinase G (PKG). Flow-induced Ca2+ influx in relation to vascular dilation and the vasodilator produced will also be discussed. © 2007 - IOS Press and the authors. All rights reserved.

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UR - https://www.scopus.com/record/pubmetrics.uri?eid=2-s2.0-34347347281&origin=recordpage

UR - https://www.webofscience.com/wos/woscc/full-record/WOS:000249052700008

M3 - RGC 21 - Publication in refereed journal

C2 - 17641396

SN - 1386-0291

VL - 37

SP - 63

EP - 70

JO - Clinical Hemorheology and Microcirculation

JF - Clinical Hemorheology and Microcirculation

IS - 1-2

ER -