Activation of the renin-angiotensin system in anti-glomerular basement membrane antibody-induced glomerulonephritis.

Authors: Yayama, K  Matsui, T  Takano, M  Hayashi, K  Nagamatsu, T  Suzuki, Y  Okamoto, H 
Citation: Yayama K, etal., Biol Pharm Bull. 1995 Mar;18(3):411-5.
Pubmed: (View Article at PubMed) PMID:7550093

Activity of the renin-angiotensin system in the nephrotic syndrome was investigated in rats with acute nephritis induced by anti-glomerular basement membrane (GBM) antibody. Injection of anti-GBM antibody resulted in a transient 2-fold elevation of both plasma renin and angiotensinogen with a peak at 12 h. Angiotensinogen mRNA levels in the liver also rapidly and transiently increased 4-fold at 3 h. The manifestation of acute nephritis, indicated by proteinuria, hypoalbuminemia, hypercholesterolemia and an increase in serum creatinine, following injection of anti-GBM antibody, was inhibited by a single administration of the selective angiotensin II type 1 receptor antagonist TCV-116 (1 mg/kg, p.o.) 2 h before an injection with the antibody, but not by successive administration of this drug for 1 week from 3 d after the injection of antibody. These results suggested that the enhanced generation of angiotensin II by elevated levels of both renin and its substrate in the early phase of anti-GBM nephritis promotes the evolution of acute nephritis via angiotensin II type 1 receptor.


Disease Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 11039051
Created: 2016-03-01
Species: All species
Last Modified: 2016-03-01
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.