scholarly journals Effects of exendin-4 on the intrarenal renin-angiotensin system and interstitial fibrosis in unilateral ureteral obstruction mice: Exendin-4 and unilateral ureteral obstruction

Author(s):  
Y. Le ◽  
Z. Zheng ◽  
J. Xue ◽  
M. Cheng ◽  
M. Guan ◽  
...  
1993 ◽  
Vol 44 (2) ◽  
pp. 390-400 ◽  
Author(s):  
J. Luis Pimentel ◽  
Manuel Martinez-Maldonado ◽  
Josiah N. Wilcox ◽  
Susheng Wang ◽  
Chuying Luo

1995 ◽  
Vol 48 (4) ◽  
pp. 1247-1253 ◽  
Author(s):  
J. Luis Pimentel ◽  
Ángel Montero ◽  
Susheng Wang ◽  
Igor Yosipiv ◽  
Samir El-Dahr ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0148542 ◽  
Author(s):  
Marilena Gregorini ◽  
Valeria Corradetti ◽  
Chiara Rocca ◽  
Eleonora Francesca Pattonieri ◽  
Teresa Valsania ◽  
...  

1995 ◽  
Vol 269 (4) ◽  
pp. F491-F499 ◽  
Author(s):  
E. A. Burdmann ◽  
T. F. Andoh ◽  
C. C. Nast ◽  
A. Evan ◽  
B. A. Connors ◽  
...  

The pathogenesis of renal scarring in chronic cyclosporin nephropathy is unknown. In this study, we evaluated the effects of renin-angiotensin system blockade by enalapril and losartan in a salt-dependent model of cyclosporin-associated chronic tubulointerstitial fibrosis (TIF). Rats kept on normal or low-salt diet were given cyclosporin, cyclosporin+enalapril, cyclosporin+losartan, cyclosporin+enalapril#losartan, or vehicle for 14 and 28 days. Cyclosporin reduced glomerular filtration rate (GFR) in rats fed either diet, but only salt-depleted animals developed significant TIF. Cyclosporin also impaired renal concentrating ability and caused tubular enzymuria. Renin-angiotensin system blockade decreased blood pressure (BP) and promoted afferent arteriolar vasodilatation. Losartan reduced plasma renin activity and prevented cyclosporin-induced increment of cortical alpha 1(I) procollagen mRNA. Renin-angiotensin blockade did not improve GFR and tubular function; however, it strikingly prevented TIF development, even in presence of very low BP. Rats treated with cyclosporin, hydralazine, and furosemide achieved BP values similar to losartan or enalapril groups, but there was no protection against interstitial fibrosis development. These results suggest that cyclosporin-related chronic interstitial injury is mediated by angiotensin II and that the mechanisms promoting the interstitial scarring can be dissociated from glomerular and tubular dysfunction in cyclosporin nephropathy.


2004 ◽  
Vol 66 (5) ◽  
pp. 1815-1825 ◽  
Author(s):  
Frédéric D. Debelle ◽  
Joëlle L. Nortier ◽  
Cécile P. Husson ◽  
Eric G. De Prez ◽  
Anne R. Vienne ◽  
...  

Urology ◽  
2001 ◽  
Vol 58 (2) ◽  
pp. 301-306 ◽  
Author(s):  
Semih Ayan ◽  
Jonathan A Roth ◽  
Michael R Freeman ◽  
Samuel H Bride ◽  
Craig A Peters

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