Key result
Cardiomyocyte-restricted GC-A deletion in mice caused mild cardiac hypertrophy, increased ANP mRNA fivefold, lowered blood pressure by 7-10 mmHg, and enhanced responses to aortic constriction.
Why the study?
Does the local ANP/GC-A system modulate cardiomyocyte growth and cardiac hypertrophy independently of systemic blood pressure?
Population
Mice with cardiomyocyte-restricted inactivation of the atrial natriuretic peptide receptor guanylyl…
Comparison
Cardiomyocyte-restricted GC-A deletion, with and… vs Normal/wild-type mice
Design
Preclinical
Authors
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Cardiomyocyte GC-A loss may drive hypertrophy independently of pressure; leaves open therapeutic targeting of local ANP signaling in hypertension.
Does the local ANP/GC-A system modulate cardiomyocyte growth and cardiac hypertrophy independently of systemic blood pressure?
The local ANP/GC-A system plays a crucial role in moderating the molecular program of cardiac hypertrophy independently of systemic blood pressure.
Holtwick et al. (2003) studied Cardiac hypertrophy. Cardiomyocyte-restricted inactivation of the GC-A gene vs. Normal mice was evaluated on Cardiac hypertrophy and mRNA expression of cardiac hypertrophy markers. Cardiomyocyte-restricted GC-A deletion in mice caused mild cardiac hypertrophy, increased ANP mRNA fivefold, lowered blood pressure by 7-10 mmHg, and enhanced responses to aortic constriction.
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