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Increased natriuretic peptide receptor A and C gene expression in rats with pressure-overload cardiac hypertrophy.

Authors: Christoffersen, TE  Aplin, M  Strom, CC  Sheikh, SP  Skott, O  Busk, PK  Haunso, S  Nielsen, LB 
Citation: Christoffersen TE, etal., Am J Physiol Heart Circ Physiol. 2006 Apr;290(4):H1635-41. Epub 2005 Nov 4.
Pubmed: (View Article at PubMed) PMID:16272201
DOI: Full-text: DOI:10.1152/ajpheart.00612.2005

Both atrial (ANP) and brain (BNP) natriuretic peptide affect development of cardiac hypertrophy and fibrosis via binding to natriuretic peptide receptor (NPR)-A in the heart. A putative clearance receptor, NPR-C, is believed to regulate cardiac levels of ANP and BNP. The renin-angiotensin system also affects cardiac hypertrophy and fibrosis. In this study we examined the expression of genes for the NPRs in rats with pressure-overload cardiac hypertrophy. The ANG II type 1 receptor was blocked with losartan (10 to investigate a possible role of the renin-angiotensin system in regulation of natriuretic peptide and NPR gene expression. The ascending aorta was banded in 84 rats during Hypnorm/Dormicum-isoflurane anesthesia; after 4 wk the rats were randomized to treatment with losartan or placebo. The left ventricle of the heart was removed 1, 2, or 4 wk later. Aortic banding increased left ventricular expression of NPR-A and NPR-C mRNA by 110% (P < 0.001) and 520% (P < 0.01), respectively, after 8 wk; as expected, it also increased the expression of ANP and BNP mRNAs. Losartan induced a slight reduction of left ventricular weight but did not affect the expression of mRNAs for the natriuretic peptides or their receptors. Although increased gene expression does not necessarily convey a higher concentration of the protein, the data suggest that pressure overload is accompanied by upregulation of not only ANP and BNP but also their receptors NPR-A and NPR-C in the left ventricle.


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CRRD Object Information
CRRD ID: 1580154
Created: 2006-06-28
Species: All species
Last Modified: 2006-06-28
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.