Hypertension is the primary cause of cardiovascular mortality. Despite multiple existing treatments, only half of those with the disease achieve adequate control. Therefore, understanding the mechanisms causing hypertension is essential for the development of novel therapies. Many studies demonstrate that immune cell infiltration of the vessel wall, kidney and central nervous system, as well as their counterparts of oxidative stress, the renal renin‐angiotensin system (RAS) and sympathetic tone play a critical role in the development of hypertension. Genetically modified mice lacking components of innate and/or adaptive immunity confirm the importance of chronic inflammation in hypertension and its complications. Depletion of immune cells improves endothelial function, decreases oxidative stress, reduces vascular tone and prevents renal interstitial infiltrates, sodium retention and kidney damage. Moreover, the ablation of microglia or central nervous system perivascular macrophages reduces RAS‐induced inflammation and prevents sympathetic nervous system activation and hypertension. Therefore, understanding immune cell functioning and their interactions with tissues that regulate hypertensive responses may be the future of novel antihypertensive therapies.

中文翻译：

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免疫和高血压。

高血压是心血管死亡的主要原因。尽管有多种现有的治疗方法，但只有一半的疾病患者能够得到足够的控制。因此，了解引起高血压的机制对于开发新疗法至关重要。许多研究表明，血管壁、肾脏和中枢神经系统的免疫细胞浸润，以及其对应的氧化应激、肾素-血管紧张素系统 (RAS) 和交感神经张力在高血压的发展中起关键作用。缺乏先天和/或适应性免疫成分的转基因小鼠证实了慢性炎症在高血压及其并发症中的重要性。免疫细胞的消耗改善内皮功能，减少氧化应激，降低血管张力并防止肾间质浸润、钠潴留和肾损伤。此外，小胶质细胞或中枢神经系统血管周围巨噬细胞的消融可减少 RAS 诱导的炎症并防止交感神经系统激活和高血压。因此，了解免疫细胞功能及其与调节高血压反应的组织的相互作用可能是新型抗高血压疗法的未来。