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December 22, 1998Proceedings of the National Academy of Sciences318 citationsOpen Access

Reduced growth, abnormal kidney structure, and type 2 (AT 2 ) angiotensin receptor-mediated blood pressure regulation in mice lacking both AT 1A and AT 1B receptors for angiotensin II

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Population

Mice lacking AT1B and both AT1A and AT1B receptors, as well as wild-type and Agtr1a -/- mice.

Comparison

Targeted disruption of Agtr1a and Agtr1b genes… vs Wild-type mice and single knockout mice.

Design

Preclinical

Authors

MOMichael I. OliverioHKHyung‐Suk KimMIMasaki Ito

Discussion

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Overview

Caution against extrapolating AT1 double-knockout phenotypes to patients; leaves open isoform compensation in human RAS.

Structured PICO

P
Population
Mice lacking AT1B (Agtr1b -/-) and both AT1A and AT1B receptors (Agtr1a -/- Agtr1b -/-), as well as wild-type and Agtr1a -/- mice.
I
Intervention
Targeted disruption of Agtr1a and Agtr1b genes (genetic knockout), and administration of angiotensin II, epinephrine, and enalapril.
C
Comparator
Wild-type mice and single knockout mice (Agtr1a -/- or Agtr1b -/-).
O
Outcome
Growth (body and organ weights), kidney histomorphology, urinary concentrating capacity, and blood pressure response to angiotensin II and enalapril.surrogate

The combined absence of AT1A and AT1B receptors in mice results in impaired growth, abnormal kidney structure, and reduced blood pressure, demonstrating that both isoforms mediate the classical functions of the renin-angiotensin system and can compensate for each other.

Cite This Study

Oliverio et al. (1998) studied this question.

synapsesocial.com/papers/6a100522b6f5ee0401603354https://doi.org/10.1073/pnas.95.26.15496
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