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February 1, 2000Journal of Hypertension

An intact renin – angiotensin system is a prerequisite for normal renal development

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Why the study?

Does interruption of the renin-angiotensin system during nephrogenesis cause renal abnormalities in experimental animal models?

Population

Experimental animal models (including mice) with ongoing nephrogenesis

Design

Review

Authors

GGGregor GuronUniversity of GothenburgPFPeter FribergPreventive Cardiology

Discussion

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Implication

Supports RAS inhibitor avoidance in pregnancy; leaves open human translation of animal renal development data.

Structured PICO

Does interruption of the renin-angiotensin system during nephrogenesis cause renal abnormalities in experimental animal models?

P
Population
Experimental animal models (including mice) with ongoing nephrogenesis
I
Intervention
Pharmacological interruption of the renin-angiotensin system or targeted inactivation of genes encoding angiotensinogen, ACE, or AT1/AT2 receptors
O
Outcome
Renal morphological and functional abnormalities (e.g., papillary atrophy, abnormal wall thickening of intrarenal arterioles, tubular atrophy, impaired urinary concentrating ability)surrogate

This review highlights that an intact renin-angiotensin system is essential for normal renal development, as its interruption in animal models leads to significant structural and functional renal abnormalities.

Cite This Study

Guron et al. (2000) studied this question.

synapsesocial.com/papers/6a71f05335aa2c282ce30241https://doi.org/10.1097/00004872-200018020-00001
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Also Consider

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  1. 1Ontogeny of somatic angiotensin-converting enzyme.1994 · 78 citations
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  3. 3Mechanisms of impaired urinary concentrating ability in adult rats treated neonatally with enalapril1999 · 50 citations
  4. 4Molecular cloning of a novel angiotensin II receptor isoform involved in phosphotyrosine phosphatase inhibition.1993 · 716 citations
  5. 5Vascular smooth muscle cell hypertrophy vs. hyperplasia. Autocrine transforming growth factor-beta 1 expression determines growth response to angiotensin II.1992 · 646 citations