Department of Pharmacology and Toxicology, Brody School of Medicine at East Carolina University, 600 Moye Blvd., Greenville, NC 27864, USA.
Pharmacol Res. 2020 May;155:104715. doi: 10.1016/j.phrs.2020.104715. Epub 2020 Feb 19.
Kinins are a family of oligopeptides of the kallikrein-kinin system that act as potent vasoactive hormones and inflammatory mediators. The bioactive kinins mainly consist of bradykinin and kallidin, and their metabolites des-Arg-bradykinin and des-Arg-kallidin. Physiological effects of kinins are mediated by activation of highly selective G-protein coupled kinin B1 and B2 receptors. Growing evidence suggests that B1 receptor activation mediates diverse physiological and pathological features of cardiovascular diseases. However, studies are limited regarding the impact of B1 receptor mediated neuroinflammation on the development of hypertension and other cardiovascular diseases. Given the potential role for B1 receptor activation in immune cell infiltration, microglia activation, and cytokine production within the central nervous system, B1 receptor mediated signaling cascades might result in elevated neuroinflammation. In this review, we will discuss the potential pro-inflammatory role of B1 receptor activation in hypertension. A better understanding of B1 receptor inflammatory signaling may lead to the development of therapeutics that target B1 receptors to treat neurogenic hypertension.
激肽是激肽释放酶-激肽系统中的一类寡肽，作为有效的血管活性激素和炎症介质发挥作用。生物活性激肽主要由缓激肽和血管舒缓素组成，其代谢产物为 des-Arg-缓激肽和 des-Arg-血管舒缓素。激肽的生理作用是通过激活高度选择性的 G 蛋白偶联激肽 B1 和 B2 受体来介导的。越来越多的证据表明，B1 受体的激活介导了心血管疾病的多种生理和病理特征。然而，关于 B1 受体介导的神经炎症对高血压和其他心血管疾病发展的影响的研究还很有限。鉴于 B1 受体激活在中枢神经系统免疫细胞浸润、小胶质细胞激活和细胞因子产生中的潜在作用，B1 受体介导的信号级联可能导致神经炎症的升高。在这篇综述中，我们将讨论 B1 受体激活在高血压中的潜在促炎作用。更好地了解 B1 受体炎症信号可能会导致开发针对 B1 受体的治疗方法，以治疗神经性高血压。
