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背景TRV l20027是ATl受体的一种新β-arrestin biased配体,但与传统的ATl受体拮抗剂不同,它参与β-arrestin介导的信号转导。TRV l20027抑制血管紧张素介导的血管收缩,经与β-arrestin结合,增加心肌细胞的收缩。作者假设:在实验性心力衰竭(简称心衰)中,TRVl20027于速尿基础上加用,有利于心、肾。方法及结果两组麻醉狗(每组6只)快速起搏致心衰。基线清除后,一组(F+V)给予速尿(1 mg.kg-1.h-1)加生理
Background TRV1220027 is a novel beta-arrestin biased ligand for the AT1 receptor, but unlike traditional AT1 receptor antagonists, it is involved in beta-arrestin-mediated signaling. TRV l20027 inhibits angiotensin-mediated vasoconstriction and increases cardiomyocyte contractions by binding to beta-arrestin. The authors hypothesized that in experimental heart failure (HF), TRVl20027 was added on the basis of furosemide, favoring the heart and kidneys. Methods and Results Two groups of anesthetized dogs (6 in each group) caused by rapid paced heart failure. After baseline clearance, one group (F + V) was given furosemide (1 mg.kg-1.h-1) plus physiology