Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1996 Sep:23 Suppl 3:S88-92.
doi: 10.1111/j.1440-1681.1996.tb02819.x.

Angiotensin receptors and development: the kidney

Affiliations
Review

Angiotensin receptors and development: the kidney

D Alcorn et al. Clin Exp Pharmacol Physiol. 1996 Sep.

Abstract

1. This brief review examines the evidence that angiotensin II (AngII) is essential for kidney development. 2. Several components of the renin-angiotensin system (RAS) are detected in the foetal kidney early in development. 3. Angiotensin II is essential for normal foetal and neonatal renal function. 4. Angiotensin II receptors transduce important signals leading to growth and development. 5. Angiotensin receptor subtypes show spatial and temporal specificity of localization throughout renal development. 6. Angiotensin converting enzyme (ACE) inhibition or AngII receptor blockade (specifically AT(1) subtype blockade) results in functional and structural abnormalities of the developing kidney in both experimental and clinical situations. 7. While chronic postnatal RAS blockade in rats is associated with structural damage to tubules and blood vessels of the kidney, reports differ on whether treatment also affects glomerular induction and growth. 8. In metanephric organ culture, glomerular induction proceeds despite AngII receptor blockade. 9. In summary, the evidence suggests that AngII is not essential for nephron induction and glomerular development in the rat kidney. However, AngII is essential for normal growth and development of renal tubules and vasculature.

PubMed Disclaimer

Publication types

MeSH terms

Substances

LinkOut - more resources