The machinery of healthy vasoconstriction: an overview.

IF 2.9 4区 医学 Q2 PHYSIOLOGY
Jana Pourová, Patrícia Dias, Milan Pour, Přemysl Mladěnka
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引用次数: 0

Abstract

Tissue perfusion is acutely regulated by the changes in the vascular tone resulting in vasodilatation or vasoconstriction (there are also long-term changes in tissue perfusion, effectively accomplished by vascular remodeling). Even though vasodilatation predominates under physiological conditions, vasoconstriction represents an essential part of normal vascular physiology. The process of vasoconstriction is very complex, being influenced by many mediators, some of which are produced by the adjacent endothelial cells. The purpose of this review is to provide an overview of the machinery of vasoconstriction addressing the main components. First, the role of calcium is discussed including its intracellular and extracellular sources, its principal function in smooth muscle contraction machinery and mechanisms counteracting its effects. Subsequently, protein kinase C is included with its activation, effects and feedback. The role of RhoA/ROCK system is addressed in a similar way. The next section deals with the role of vascular endothelium-derived contracting factors and their effects on the adjacent smooth muscle cells. Finally, principal mechanisms of action of vasoconstrictive stimuli and myogenic tone are concisely discussed.

健康血管收缩机制综述
组织灌注受血管张力变化引起的血管舒张或收缩的急性调节(组织灌注也存在长期变化,通过血管重塑有效地完成)。尽管血管扩张在生理条件下占主导地位,血管收缩是正常血管生理的重要组成部分。血管收缩的过程是非常复杂的,受许多介质的影响,其中一些是由邻近的内皮细胞产生的。这篇综述的目的是提供血管收缩机制的概述,包括主要成分。首先,本文讨论了钙的作用,包括其细胞内和细胞外来源,其在平滑肌收缩机制中的主要功能和抵消其影响的机制。随后,包括蛋白激酶C及其激活、作用和反馈。RhoA/ROCK系统的作用以类似的方式处理。下一节讨论血管内皮源性收缩因子的作用及其对邻近平滑肌细胞的影响。最后,简要讨论了血管收缩刺激和肌张力的主要作用机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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