Lady Davis Institute for Medical Research and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montréal, Québec, Canada.
Can J Cardiol. 2020 May;36(5):648-658. doi: 10.1016/j.cjca.2020.02.003. Epub 2020 Feb 8.
Large conduit arteries and the microcirculation participate in the mechanisms of elevation of blood pressure (BP). Large vessels play roles predominantly in older subjects, with stiffening progressing after middle age leading to increases in systolic BP found in most humans with aging. Systolic BP elevation and increased pulsatility penetrate deeper into the distal vasculature, leading to microcirculatory injury, remodelling, and associated endothelial dysfunction. The result is target organ damage in the heart, brain, and kidney. In younger individuals genetically predisposed to high BP, increased salt intake or other exogenous or endogenous risk factors for hypertension, including overweight and excess alcohol intake, lead to enhanced sympathetic activity and vasoconstriction. Enhanced vasoconstrictor responses and myogenic tone become persistent when embedded in an increased extracellular matrix, resulting in remodelling of resistance arteries with a narrowed lumen and increased media-lumen ratio. Stimulation of the renin-angiotensin-aldosterone and endothelin systems and inflammatory and immune activation, to which gut microbiome dysbiosis may contribute as a result of salt intake, also participate in the injury and remodelling of the microcirculation and endothelial dysfunction. Inflammation of perivascular fat and loss of anticontractile factors play roles as well in microvessel remodelling. Exaggerated myogenic tone leads to closure of terminal arterioles, collapse of capillaries and venules, functional rarefaction, and eventually to anatomic rarefaction, compromising tissue perfusion. The remodelling of the microcirculation raises resistance to flow, and accordingly raises BP in a feedback process that over years results in stiffening of conduit arteries and systo-diastolic or predominantly systolic hypertension and, more rarely, predominantly diastolic hypertension. Thus, at different stages of life and the evolution of hypertension, large vessels and the microcirculation interact to contribute to BP elevation.
大的管道动脉和微循环参与了血压升高的机制。大动脉主要在老年患者中起作用，从中年以后，血管变硬会导致大多数老年人的收缩压升高。收缩压升高和脉动增加会渗透到更远端的血管系统，导致微血管损伤、重塑和相关的内皮功能障碍。其结果是心脏、大脑和肾脏等靶器官受损。在易患高血压的年轻个体中，遗传因素、高盐摄入或其他高血压的外源性或内源性危险因素，包括超重和过量饮酒，会导致交感神经活性和血管收缩增强。当嵌入到增加的细胞外基质中时，增强的血管收缩反应和肌源性张力会持续存在，导致阻力血管的重塑，管腔变窄，中膜-腔比增加。肾素-血管紧张素-醛固酮和内皮素系统的刺激以及炎症和免疫激活也参与了微循环和内皮功能障碍的损伤和重塑。血管周围脂肪的炎症和抗收缩因子的丧失也在微血管重塑中起作用。过度的肌源性张力导致终末小动脉闭塞、毛细血管和小静脉塌陷、功能性稀疏，最终导致解剖学稀疏，从而损害组织灌注。微循环的重塑增加了血流阻力，因此在反馈过程中会升高血压，随着时间的推移，会导致大血管变硬以及收缩期-舒张期或主要是收缩期高血压，更罕见的是，主要是舒张期高血压。因此，在生命的不同阶段和高血压的演变过程中，大血管和微循环相互作用，导致血压升高。
