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摘要
肾素血管紧张素醛固酮系统(RAAS)的生理功能可维持心血管系统的稳态。在病理生理条件下,过度激活的RAAS会导致血管紧张素II(AngII)的浓度增加,以及过度激活的血管紧张素1型受体(AT1R),导致血管收缩,钠潴留和心肌细胞生长变化。它会引起心脏的心脏重塑,从而导致左心室肥大,扩张和功能障碍,最终导致心力衰竭(HF)。使用血管紧张素转化酶抑制剂(ACEi)或血管紧张素受体阻滞剂(ARB)抑制RAAS已显示可显着降低因HF引起的发病率和死亡率。与ARB相比,由于不适,ACEi已显示出较高的停药率。因此,ARB是与其他抗高血压药联合治疗HF的医生的首选。目前,有8种ARB已获得FDA批准并投入临床使用。即使它们与取代AngII的AT1R的同一位点结合,但临床结果却有显着差异。在这篇综述中,我们描述了每种ARB在治疗HF中的临床意义及其临床结果。
关键词: AT1R,AngII,血管紧张素受体阻滞剂,心力衰竭,心血管疾病,高血压,GPCR。
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