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[缺氧性肺血管收缩期间血管平滑肌细胞的钙敏感性]

[Calcium sensitivity in vascular smooth muscle cell during hypoxic pulmonary vasoconstriction].

作者信息

Koubský K

出版信息

Cesk Fysiol. 2015;64(1):19-22.

PMID:26738243
Abstract

Hypoxic pulmonary vasoconstriction is a means of optimising the oxygenation of blood in the lungs by redistributing the flow from poorly ventilated areas into well ventilated ones. It is caused by a direct effect of hypoxia on pulmonary vascular smooth muscle cells. For a vascular smooth muscle cell to contract, an increased intracellular concentration of calcium is needed. However, the contraction force can also be regulated independently of calcium concentration by calcium sensitivity. The sensitivity is regulated mainly by activation/deactivation of myosin light chain phosphatase. Several metabolic pathways converge on this enzyme. The increase in calcium sensitivity is an important process during hypoxic pulmonary vasoconstriction.

摘要

缺氧性肺血管收缩是一种通过将血流从通气不良区域重新分配到通气良好区域来优化肺部血液氧合的方式。它是由缺氧对肺血管平滑肌细胞的直接作用引起的。血管平滑肌细胞要收缩,就需要细胞内钙浓度增加。然而,收缩力也可以通过钙敏感性独立于钙浓度进行调节。这种敏感性主要由肌球蛋白轻链磷酸酶的激活/失活来调节。几种代谢途径都作用于这种酶。钙敏感性增加是缺氧性肺血管收缩过程中的一个重要过程。

相似文献

1
[Calcium sensitivity in vascular smooth muscle cell during hypoxic pulmonary vasoconstriction].[缺氧性肺血管收缩期间血管平滑肌细胞的钙敏感性]
Cesk Fysiol. 2015;64(1):19-22.
2
Protein kinases in vascular smooth muscle tone--role in the pulmonary vasculature and hypoxic pulmonary vasoconstriction.血管平滑肌张力中的蛋白激酶——在肺血管系统及低氧性肺血管收缩中的作用
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3
Point: release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction.观点:内皮源性血管收缩因子的释放以及RhoA/Rho激酶介导的平滑肌细胞收缩的钙敏化作用是/不是完全且持续的低氧性肺血管收缩的主要效应机制。
J Appl Physiol (1985). 2007 May;102(5):2071-2; discussion 2075-6. doi: 10.1152/japplphysiol.01258.2006. Epub 2006 Nov 9.
4
Hypoxic pulmonary vasoconstriction: cyclic adenosine diphosphate-ribose, smooth muscle Ca(2+) stores and the endothelium.缺氧性肺血管收缩:环磷酸腺苷二磷酸核糖、平滑肌钙(2+)储备与内皮
Respir Physiol Neurobiol. 2002 Aug 22;132(1):3-15. doi: 10.1016/s1569-9048(02)00046-0.
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Point:Counterpoint: "Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction".观点:对立观点:“内皮源性血管收缩剂的释放以及RhoA/Rho激酶介导的平滑肌细胞收缩钙敏化是/不是完全且持续的低氧性肺血管收缩的主要效应器” 。
J Appl Physiol (1985). 2007 May;102(5):2077; discussion 2080. doi: 10.1152/japplphysiol.01435.2006.
6
Hypoxic pulmonary vasoconstriction: mechanisms and controversies.缺氧性肺血管收缩:机制与争议
J Physiol. 2006 Jan 1;570(Pt 1):53-8. doi: 10.1113/jphysiol.2005.098855. Epub 2005 Oct 27.
7
Rho-kinase activation is involved in hypoxia-induced pulmonary vasoconstriction.Rho激酶激活参与缺氧诱导的肺血管收缩。
Am J Respir Cell Mol Biol. 2001 Nov;25(5):628-35. doi: 10.1165/ajrcmb.25.5.4461.
8
Point:Counterpoint "Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction".正方观点对反方观点:“内皮源性血管收缩因子的释放以及RhoA/Rho激酶介导的平滑肌细胞收缩钙敏化是/不是完全且持续的低氧性肺血管收缩的主要效应器”
J Appl Physiol (1985). 2007 May;102(5):2078; discussion 2080. doi: 10.1152/japplphysiol.01435.2006.
9
Point:Counterpoint "Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction".正方观点对反方观点:“内皮源性血管收缩因子的释放以及RhoA/Rho激酶介导的平滑肌细胞收缩钙敏化是/不是完全且持续的低氧性肺血管收缩的主要效应器”
J Appl Physiol (1985). 2007 May;102(5):2078-9; discussion 2080. doi: 10.1152/japplphysiol.01435.2006.
10
Point:Counterpoint "Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction".正方观点:反方观点 “内皮源性血管收缩因子的释放以及RhoA/Rho激酶介导的平滑肌细胞收缩钙敏化是/不是完全性和持续性低氧性肺血管收缩的主要效应器”。
J Appl Physiol (1985). 2007 May;102(5):2077-8; discussion 2080. doi: 10.1152/japplphysiol.01435.2006.