Key result
Transgenic mice overexpressing an AT1 receptor mutant lacking Gq/Gi coupling developed more severe cardiac hypertrophy and bradycardia coupled with lower cardiac function than mice overexpressing the wild-type AT1 receptor.
Why the study?
Does cardiac-specific overexpression of an AT1 receptor mutant lacking Gq/Gi coupling induce cardiac hypertrophy and bradycardia in transgenic mice?
Population
Transgenic mice with cardiac-specific overexpression of WT AT1 receptor or an AT1 receptor second…
Comparison
Cardiac-specific overexpression of AT1-i2m. vs Cardiac-specific overexpression of AT1-WT and…
Design
Preclinical
Follow-up
Up to 18 months
Authors
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Gq/Gi-independent AT1 signaling may promote severe hypertrophy and dysfunction in mice; leaves open relevance to human cardiomyopathy.
Does cardiac-specific overexpression of an AT1 receptor mutant lacking Gq/Gi coupling induce cardiac hypertrophy and bradycardia in transgenic mice?
Absolute Event Rate: 4.51% vs 3.49%
p-value: p=<0.05
The AT1 receptor mediates downstream signaling through Gq/Gi-independent mechanisms that induce a distinct phenotype of severe cardiac hypertrophy and bradycardia in vivo.
Peiyong Zhai (2005) studied Cardiac hypertrophy and bradycardia. Cardiac-specific overexpression of AT1-i2m (mutant lacking Gq/Gi coupling) vs. Overexpression of AT1-WT and non-transgenic mice was evaluated on Left ventricular weight to body weight ratio (LVW/BW) (p=<0.05). Transgenic mice overexpressing an AT1 receptor mutant lacking Gq/Gi coupling developed more severe cardiac hypertrophy and bradycardia coupled with lower cardiac function than mice overexpressing the wild-type AT1 receptor.
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