Pourová Jana, Dias Patrícia, Pour Milan, Mladěnka Přemysl
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Charles University, Akademika Heyrovskeho 1203, 500 05, Hradec Kralove, Czech Republic.
Frick Center for Heart Failure and Arrhythmia, Dorothy M. Davis Heart and Lung Research Institute, College of Medicine, Ohio State University Wexner Medical Center, Columbus, OH, USA.
Pflugers Arch. 2025 Jul 11. doi: 10.1007/s00424-025-03103-6.
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.
组织灌注通过血管张力的变化进行急性调节,导致血管舒张或收缩(组织灌注也存在长期变化,可通过血管重塑有效实现)。尽管在生理条件下血管舒张占主导,但血管收缩是正常血管生理的重要组成部分。血管收缩过程非常复杂,受许多介质影响,其中一些由相邻的内皮细胞产生。本综述的目的是概述血管收缩机制,涉及主要组成部分。首先,讨论钙的作用,包括其细胞内和细胞外来源、在平滑肌收缩机制中的主要功能以及抵消其作用的机制。随后,介绍蛋白激酶C及其激活、作用和反馈。以类似方式阐述RhoA/ROCK系统的作用。下一部分讨论血管内皮衍生的收缩因子的作用及其对相邻平滑肌细胞的影响。最后,简要讨论血管收缩刺激和肌源性张力的主要作用机制。