Endothelin in Nondiabetic Chronic Kidney Disease: Preclinical and Clinical Studies

被引:14
作者
Culshaw, Geoff J. [1 ]
MacIntyre, Iain M. [1 ]
Dhaun, Neeraj [1 ]
Webb, David J. [1 ]
机构
[1] Univ Edinburgh, Univ British Heart Fdn, Ctr Cardiovasc Sci, Queens Med Res Inst, Edinburgh EH16 4TJ, Midlothian, Scotland
关键词
Chronic kidney disease; endothelin; endothelin-receptor antagonist; proteinuria; blood pressure; A RECEPTOR ANTAGONISM; DUCT-SPECIFIC KNOCKOUT; NOCTURNAL BLOOD-PRESSURE; ANGIOTENSIN-II; CARDIOVASCULAR-DISEASE; ARTERIAL STIFFNESS; CONVERTING ENZYME; PODOCYTE INJURY; RENAL-DISEASE; VASA-RECTA;
D O I
10.1016/j.semnephrol.2015.03.002
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The incidence and prevalence of chronic kidney disease (CKD) is increasing. Despite current therapies, many patients with CKD have suboptimal blood pressure, ongoing proteinuria, and develop progressive renal dysfunction. Further therapeutic options therefore are required. Over the past 20 years the endothelin (ET) system has become a prime target. Experimental models have shown that ET-1, acting primarily via the endothelin-A receptor, plays an important role in the development of proteinuria, glomerular injury, fibrosis, and inflammation. Subsequent animal and early clinical studies using ET-receptor antagonists have suggested that theses therapies may slow renal disease progression primarily through blood pressure and proteinuria reduction. This review examines the current literature regarding the ET system in nondiabetic CKD. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:176 / 187
页数:12
相关论文
共 122 条
[1]   ROLE OF NEUTRAL ENDOPEPTIDASE IN THE METABOLISM OF ENDOTHELIN [J].
ABASSI, ZA ;
TATE, JE ;
GOLOMB, E ;
KEISER, HR .
HYPERTENSION, 1992, 20 (01) :89-95
[2]  
ACHMAD TH, 1992, BIOCHEM BIOPH RES CO, V189, P994
[3]   The regulation of blood perfusion in the renal cortex and medulla by reactive oxygen species and nitric oxide in the anaesthetised rat [J].
Ahmeda, A. F. ;
Johns, E. J. .
ACTA PHYSIOLOGICA, 2012, 204 (03) :443-450
[4]   Collecting duct-specific knockout of endothelia-1 causes hypertension and sodium retention [J].
Ahn, D ;
Ge, YQ ;
Stricklett, PK ;
Gill, P ;
Taylor, D ;
Hughes, AK ;
Yanagisawa, M ;
Miller, L ;
Nelson, RD ;
Kohan, DE .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (04) :504-511
[5]  
[Anonymous], 2014, CHRON KIDN DIS EARL
[6]   Endothelin peptide and receptors in human atherosclerotic coronary artery and aorta [J].
Bacon, CR ;
Cary, NR ;
Davenport, AP .
CIRCULATION RESEARCH, 1996, 79 (04) :794-801
[7]   Angiotensin II increases vascular and renal endothelin-1 and functional endothelin converting enzyme activity in vivo: Role of ETA receptors for endothelin regulation [J].
Barton, M ;
Shaw, S ;
dUscio, LV ;
Moreau, P ;
Luscher, TF .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 238 (03) :861-865
[8]  
Barton M, 2011, CONTRIB NEPHROL, V172, P255, DOI 10.1159/000328859
[9]   Family History of Renal Disease Severity Predicts the Mutated Gene in ADPKD [J].
Barua, Moumita ;
Cil, Onur ;
Paterson, Andrew D. ;
Wang, Kairon ;
He, Ning ;
Dicks, Elizabeth ;
Parfrey, Patrick ;
Pei, York .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2009, 20 (08) :1833-1838
[10]   A SPECIFIC ENDOTHELIN SUBTYPE-A RECEPTOR ANTAGONIST PROTECTS AGAINST INJURY IN RENAL-DISEASE PROGRESSION [J].
BENIGNI, A ;
ZOJA, C ;
CORNA, D ;
ORISIO, S ;
LONGARETTI, L ;
BERTANI, T ;
REMUZZI, G .
KIDNEY INTERNATIONAL, 1993, 44 (02) :440-444