Key result
Null mutation of the angiotensin type 1B receptor gene in mice resulted in intact microscopic anatomy, comparable systemic blood pressure, and comparable plasma aldosterone levels to wild-type mice.
Population
6- to 8-wk-old mice
Comparison
Null mutation of the mouse angiotensin type 1B… vs Wild-type mice (Agtr1b +/+)
Design
Preclinical
Authors
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AT1B deletion yields no overt phenotype in mice; leaves open compensatory AT1A roles or species-specific functions requiring human validation.
Targeted deletion of the AT1B receptor gene in mice does not result in abnormal phenotypes, suggesting AT1A receptors may compensate or other non-AT1/AT2 receptors exist.
Chen et al. (1997) studied this question. Null mutation of the mouse angiotensin type 1B (AT1B) receptor gene (Agtr1b) vs. Agtr1b +/+ mice (wild-type) was evaluated on Systemic blood pressure, plasma aldosterone level, and microscopic anatomy. Null mutation of the angiotensin type 1B receptor gene in mice resulted in intact microscopic anatomy, comparable systemic blood pressure, and comparable plasma aldosterone levels to wild-type mice.
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