Classic and Nonclassic Renin-Angiotensin Systems in the Critically Ill

被引：74

作者：

Bitker, Laurent ^{[1
]}

Burrell, Louise M. ^{[2
]}

机构：

[1] Austin Hosp, Dept Intens Care, ICU Res Off, 145 Studley Rd, Heidelberg, Vic 3084, Australia

[2] Univ Melbourne, Austin Hosp, Austin Hlth, Dept Med, 145 Studley Rd, Heidelberg, Vic 3084, Australia

来源：

CRITICAL CARE CLINICS | 2019年 / 35卷 / 02期

关键词：

Acute kidney injury; Acute respiratory distress syndrome; Angiotensin; Angiotensin-converting enzyme; Sepsis; Inflammation; Septic shock; Renin; CONVERTING ENZYME 2; FACTOR-KAPPA-B; RENAL BLOOD-FLOW; T-LYMPHOCYTES; ACE2; EXPRESSION; FILTRATION-RATE; CRUCIAL ROLE; LUNG INJURY; RECEPTOR; KIDNEY;

D O I：

10.1016/j.ccc.2018.11.002

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

Classic and nonclassic renin-angiotensin systems (RAS) are 2 sides of an ubiquitous endocrine/paracrine cascade regulating blood pressure and homeostasis. Angiotensin II and angiotensin-converting enzyme (ACE) levels are associated with severity of disease in the critically ill, and are central to the physiology and the pathogenesis of circulatory shock. Angiotensin (1-7) and ACE2 act as an endogenous counterregulatory arm to the angiotensin II/ACE axis. The tissue-based RAS has paracrine effects dissociated from those of the circulating RAS. Exogenous angiotensin II or ACE2 may improve the outcome of septic shock and acute respiratory distress syndrome, respectively.

引用

页码：213 / +

页数：16

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