Gene targeting in mice reveals a requirement for angiotensin in the development and maintenance of kidney morphology and growth factor regulation.
作者： F Niimura , P A Labosky , J Kakuchi , S Okubo , H Yoshida
DOI: 10.1172/JCI118366
关键词:
摘要: Elevated levels of endogenous angiotensin can cause hypertensive nephrosclerosis as a result the potent vasopressor action peptide. We have produced by gene targeting mice homozygous for null mutation in angiotensinogen (Atg-1-). Postnatally, Atg-1- animals show modest delay glomerular maturation. Although are hypotensive 7 wk age, they develop, 3 pronounced lesions renal cortex, similar to those nephrosclerosis. In addition, papillae mutant kidneys reduced size. These accompanied local up-regulation PDGF-B and TGF-beta1 mRNA cortex down-regulation PDGF-A papilla. The study demonstrates an important requirement achieving maintaining normal morphology kidney. mechanism through which maintains volume homeostasis mammals includes promotion maturational growth
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