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/ mice with cardiac
hypertrophy and fibrosis
1 Department of Medicine, Christchurch School of Medicine, Christchurch, New Zealand; and 2 Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, North Carolina 27599-7525
Atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) are cardiac hormones that regulate
blood pressure and volume, and exert their biological actions via the
natriuretic peptide receptor-A gene (Npr1). Mice lacking
Npr1 (Npr
/) have marked cardiac
hypertrophy and fibrosis disproportionate to their increased blood
pressure. This study examined the relationships between ANP and BNP
gene expression, immunoreactivity and fibrosis in cardiac tissue,
circulating ANP levels, and ANP and BNP mRNA during embryogenesis in
Npr1/ mice. Disruption of the
Npr1 signaling pathway resulted in augmented ANP and BNP
gene and ANP protein expression in the cardiac ventricles, most
pronounced for ANP mRNA in females [414 ± 57 in
Npr1/ ng/mg and 124 ± 25 ng/mg in
wild-type (WT) by Taqman assay, P < 0.001]. This
increased expression was highly correlated to the degree of cardiac
hypertrophy and was localized to the left ventricle (LV) inner free
wall and to areas of ventricular fibrosis. In contrast, plasma ANP was
significantly greater than WT in male but not female
Npr1/ mice. Increased ANP and BNP gene
expression was observed in Npr1/ embryos
from 16 days of gestation. Our study suggests that cardiac ventricular
expression of ANP and BNP is more closely associated with local
hypertrophy and fibrosis than either systemic blood pressure or
circulating ANP levels.
atrial natriuretic peptide; brain natriuretic peptide
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