There is considerable interest in traumatic brain injury (TBI) induced by repeated concussions suffered by athletes in sports, military personnel from combat-and non-combat related activities, and civilian populations who suffer head injuries from accidents and domestic violence. Although the renin-angiotensin system (RAS) is primarily a systemic cardiovascular regulatory system that, when dysregulated, causes hypertension and cardiovascular pathology, the brain contains a local RAS that plays a critical role in the pathophysiology of several neurodegenerative diseases. This local RAS includes receptors for angiotensin (Ang) II within the brain parenchyma, as well as on circumventricular organs outside the blood-brain-barrier. The brain RAS acts primarily via the type 1 Ang II receptor (AT₁R), exacerbating insults and pathology. With TBI, the brain RAS may contribute to permanent brain damage, especially when a second TBI occurs before the brain recovers from an initial injury. Agents are needed that minimize the extent of injury from an acute TBI, reducing TBI-mediated permanent brain damage. This review discusses how activation of the brain RAS following TBI contributes to this damage, and how drugs that counteract activation of the AT₁R including AT₁R blockers (ARBs), renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, and agonists at type 2 Ang II receptors (AT₂) and at Ang (1–7) receptors (Mas) can potentially ameliorate TBI-induced brain damage.

人们对运动中的运动员、从事战斗和非战斗相关活动的军事人员以及因事故和家庭暴力而头部受伤的平民反复遭受脑震荡而引起的创伤性脑损伤 (TBI) 引起了相当大的兴趣。尽管肾素-血管紧张素系统 (RAS) 主要是一个全身性心血管调节系统，当其失调时，会导致高血压和心血管病理学，但大脑中含有一种局部 RAS，它在几种神经退行性疾病的病理生理学中起关键作用。这种局部 RAS 包括脑实质内的血管紧张素 (Ang) II 受体，以及血脑屏障外的脑室周围器官上的受体。大脑 RAS 主要通过 1 型 Ang II 受体（AT ₁R），加剧侮辱和病理。对于 TBI，大脑 RAS 可能导致永久性脑损伤，尤其是在大脑从最初的损伤中恢复之前发生第二次 TBI 时。需要能够最大限度地减少急性 TBI 损伤程度、减少 TBI 介导的永久性脑损伤的药物。这篇综述讨论了 TBI 后大脑 RAS 的激活如何导致这种损伤，以及如何抵消 AT 1 R 激活的药物，_包括AT ₁ R 阻滞剂 (ARB)、肾素抑制剂、血管紧张素转换酶 (ACE) 抑制剂和激动剂2 型 Ang II 受体 (AT ₂ ) 和 Ang (1-7) 受体 (Mas) 可以潜在地改善 TBI 诱导的脑损伤。