Bestavashvili Af A, Bestavashvili Al A, Saidova A I, Shchekochikhin D Iu, Kopylov F Iu, Syrkin A L
Department of Cardiology, Functional and Ultrasound Diagnosis, Institute of Clinical Medicine, I.M. Sechenov First Moscow State Medical University, Moscow, Russia.
Moscow State University of Medicine and Dentistry named after A.I. Evdokimov, Moscow, Russia.
Angiol Sosud Khir. 2020;26(2):10-16. doi: 10.33529/ANGI02020209.
Ageing is considered to be the major and non-modifiable risk factor for the development of hypertension and cardiovascular diseases. During ageing, the vascular system undergoes structural and functional alterations, including endothelial dysfunction, thickening of the vascular wall, reduced distensibility and increased arterial stiffness. Vascular rigidity results from fibrosis and remodelling of the extracellular matrix, processes that are associated with ageing and are amplified in hypertension. These events may be induced by vasoactive agents, such as angiotensin II, endothelin-1, and aldosterone, which are increased in the vasculature during aging and hypertension. Complex interaction between the process of ageing and prohypertensive factors results in accelerated vascular remodelling and fibrosis, as well as increased arterial stiffness. Hypertension accelerates and augments age-related vascular remodelling and dysfunction, and ageing may impact on the severity of vascular damage in hypertension, thus strongly suggesting close interactions between biological ageing and blood pressure elevation. Molecular and cellular mechanisms underlying vascular alterations in ageing and hypertension are common and include aberrant signal transduction, oxidative stress and activation of pro-inflammatory and pro-fibrotic transcription factors. Strategies to suppress age-associated vascular changes can ameliorate vascular damage associated with hypertension. This article looks into vascular alterations occurring during ageing and hypertension, focussing particularly on arterial stiffness and vascular remodelling, also emphasizing the importance of diagnostic methods.
衰老被认为是高血压和心血管疾病发生的主要且不可改变的风险因素。在衰老过程中,血管系统会发生结构和功能改变,包括内皮功能障碍、血管壁增厚、扩张性降低和动脉僵硬度增加。血管僵硬是由细胞外基质的纤维化和重塑引起的,这些过程与衰老相关,且在高血压中会加剧。这些事件可能由血管活性物质诱导,如血管紧张素II、内皮素-1和醛固酮,它们在衰老和高血压过程中在血管系统中增加。衰老过程与高血压相关因素之间的复杂相互作用导致血管重塑和纤维化加速,以及动脉僵硬度增加。高血压会加速并加剧与年龄相关的血管重塑和功能障碍,而衰老可能会影响高血压中血管损伤的严重程度,因此强烈表明生物衰老与血压升高之间存在密切相互作用。衰老和高血压中血管改变的分子和细胞机制是常见的,包括异常信号转导、氧化应激以及促炎和促纤维化转录因子的激活。抑制与年龄相关的血管变化的策略可以改善与高血压相关的血管损伤。本文探讨了衰老和高血压过程中发生的血管改变,特别关注动脉僵硬度和血管重塑,同时也强调了诊断方法的重要性。