Gene targeting in mice reveals a requirement for angiotensin in the development and maintenance of kidney morphology and growth factor regulation.

F Niimura; P A Labosky; J Kakuchi; S Okubo; H Yoshida; T Oikawa; T Ichiki; A J Naftilan; A Fogo; T Inagami

doi:10.1172/JCI118366

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Niimura, F. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Labosky, P. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Kakuchi, J. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Okubo, S. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Yoshida, H. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Oikawa, T. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Ichiki, T. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Naftilan, A. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Fogo, A. in: PubMed | Google Scholar

Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Inagami, T. in: PubMed | Google Scholar

Published in Volume 96, Issue 6 on December 1, 1995
J Clin Invest. 1995;96(6):2947–2954. https://doi.org/10.1172/JCI118366.
© 1995 The American Society for Clinical Investigation

Published December 1, 1995 - Version history

Elevated levels of endogenous angiotensin can cause hypertensive nephrosclerosis as a result of the potent vasopressor action of the peptide. We have produced by gene targeting mice homozygous for a null mutation in the angiotensinogen gene (Atg-1-). Postnatally, Atg-1- animals show a modest delay in glomerular maturation. Although Atg-1- animals are hypotensive by 7 wk of age, they develop, by 3 wk of age, pronounced lesions in the renal cortex, similar to those of hypertensive nephrosclerosis. In addition, the papillae of homozygous mutant kidneys are reduced in size. These lesions are accompanied by local up-regulation of PDGF-B and TGF-beta1 mRNA in the cortex and down-regulation of PDGF-A mRNA in the papilla. The study demonstrates an important requirement for angiotensin in achieving and maintaining the normal morphology of the kidney. The mechanism through which angiotensin maintains the volume homeostasis in mammals includes promotion of the maturational growth of the papilla.

Images.

Version 1 (December 1, 1995): No description

Gene targeting in mice reveals a requirement for angiotensin in the development and maintenance of kidney morphology and growth factor regulation.

F Niimura, P A Labosky, J Kakuchi, S Okubo, H Yoshida, T Oikawa, T Ichiki, A J Naftilan, A Fogo, and T Inagami

Article tools

Metrics

Go to

Gene targeting in mice reveals a requirement for angiotensin in the development and maintenance of kidney morphology and growth factor regulation.

F Niimura, P A Labosky, J Kakuchi, S Okubo, H Yoshida, T Oikawa, T Ichiki, A J Naftilan, A Fogo, and T Inagami

Article tools

Metrics

Go to

Sign up for email alerts