The renin-angiotensin system in kidney development

被引：41

作者：

Chen, Y ^{[1
]}

Lasaitiene, D ^{[1
]}

Friberg, P ^{[1
]}

机构：

[1] Univ Gothenburg, Dept Physiol, SE-40530 Gothenburg, Sweden

来源：

ACTA PHYSIOLOGICA SCANDINAVICA | 2004年 / 181卷 / 04期

关键词：

caspases; growth factors; E-cadherin; leucocytes; nephrogenesis; vasculogenesis;

D O I：

10.1111/j.1365-201X.2004.01327.x

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

All components of the renin-angiotensin system (RAS) are highly expressed in the developing kidney in a pattern suggesting a role for angiotensin II in renal development. In support of this notion, pharmacological interruption of angiotensin II type-1 (AT(1)) receptor signalling in animals with an ongoing nephrogenesis produces specific renal abnormalities characterized by papillary atrophy, abnormal wall thickening of intrarenal arterioles, tubular atrophy associated with expansion of the interstitium, and a marked impairment in urinary concentrating ability. Similar changes in renal morphology and function develop also in mice with targeted inactivation of genes encoding renin, angiotensinogen, angiotensin-converting enzyme, or both AT(1) receptor isoforms simultaneously. Taken together, these results clearly indicate that an intact signalling through AT(1) receptors is a prerequisite for normal renal development. The present report mainly reviews the renal abnormalities induced by blocking the RAS pharmacologically in experimental animal models. In addition, pathogenetic mechanisms are discussed.

引用

页码：529 / 535

页数：7

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