Document Detail


Nephrotoxicity of angiotensin inhibition during the perinatal period.
MedLine Citation:
PMID:  11053975     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
As the only ex utero mechanism for the removal of nitrogenous waste, the mammalian kidney achieves some 50-fold increase in urine production during the perinatal period when the placental circulation becomes no longer available as a functional dialyzer. This urine is efficiently removed from the kidney by the renal pelvis, a smooth muscle structure unique to mammals, which develops during the perinatal period. We found that mutant mice completely devoid of angiotensinogen or its type 1 receptor, as well as wild-type neonates given an ACE inhibitor, fail to develop a renal pelvis or a ureteral peristaltic movement. These structural and functional defects in the urinary tract are followed by severe obstructive injury of the renal parenchyma. The ability of angiotensin to directly induce the pelvis is demonstrated in an organ culture system, in which treatment with angiotensin induces the characteristic smooth muscle layer in the wild type, but not in homozygous null mutants. Upregulation of both renal angiotensin content and type 1 receptor at the renal hilum are also demonstrated in the wild type during the transition from intra- to extra-uterine life. By inducing the timely development of the renal pelvis, angiotensin thus facilitates the removal from the renal parenchyma of the urine that promptly increases at birth, thereby effectively preventing a buildup of intrarenal pressure and a consequent development of dysmorphic kidney.
Authors:
Y Miyazaki; I Ichikawa
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Experimental nephrology     Volume:  9     ISSN:  1018-7782     ISO Abbreviation:  Exp. Nephrol.     Publication Date:  2001  
Date Detail:
Created Date:  2000-11-27     Completed Date:  2000-12-07     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9302239     Medline TA:  Exp Nephrol     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  10-3     Citation Subset:  IM    
Copyright Information:
Copyright 2000 S. Karger AG, Basel.
Affiliation:
Department of Pediatrics, Vanderbilt University Medical Center Nashville, Tenn., USA.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin-Converting Enzyme Inhibitors
Angiotensinogen / deficiency
Angiotensins / antagonists & inhibitors*
Animals
Animals, Newborn / physiology*
Kidney Diseases / chemically induced,  etiology*
Kidney Pelvis / growth & development
Mice
Mice, Mutant Strains / physiology
Receptor, Angiotensin, Type 1
Receptor, Angiotensin, Type 2
Receptors, Angiotensin / deficiency
Urinary Tract / growth & development
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Angiotensins; 0/Receptor, Angiotensin, Type 1; 0/Receptor, Angiotensin, Type 2; 0/Receptors, Angiotensin; 11002-13-4/Angiotensinogen

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