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Am J Physiol Heart Circ Physiol (March 18, 2005). doi:10.1152/ajpheart.00117.2005
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Submitted on February 4, 2005
Accepted on March 15, 2005

Cardiac-Specific Attenuation of Natriuretic Peptide A Receptor Activity Accentuates Adverse Cardiac Remodeling and Mortality in Response to Pressure Overload

Jeetendra B Patel1, Maria L Valencik2, Allison M Pritchett1, John C Burnett, Jr.1, John A McDonald2, and Margaret M Redfield1*

1 Cardiorenal Research Laboratory, Mayo Clinic College of Medicine, Rochester, MN, USA
2 School of Medicine, University of Nevada, Reno, Reno, NV, USA

* To whom correspondence should be addressed. E-mail: redfield.margaret{at}mayo.edu.

Atrial (ANP) and brain (BNP) natriuretic peptides are hormones of myocardial cell origin. These hormones bind to the natriuretic peptide A receptor (NPRA) throughout the body, stimulating cGMP production and playing a key role in blood pressure control. As NPRA receptors are present on cardiomyocytes, we hypothesized that natriuretic peptides may have direct autocrine or paracrine effects on cardiomyocytes or adjacent cardiac cells. As both natriuretic peptides and NPRA gene expression are up-regulated in states of pressure overload, we speculated that the effects of the natriuretic peptides on cardiac structure and function would be most apparent after pressure overload. To attenuate cardiomyocyte NPRA activity, transgenic mice with cardiac specific expression of a dominant negative (DN-NPRA) mutation (HCAT D 893A) in the NPRA receptor were created. Cardiac structure and function were assessed (avertin anesthesia) in the absence and presence of pressure overload produced by supra-renal aortic banding. In the absence of pressure overload, basal and BNP-stimulated guanylyl cyclase activity assessed in cardiac membrane fractions was reduced. However, systolic blood pressure, myocardial cGMP, Log plasma ANP levels and ventricular structure and function were similar in wild type (WT-NPRA) and DN-NPRA mice. In the presence of pressure overload, myocardial cGMP levels were reduced and ventricular hypertrophy, fibrosis and filling pressures and mortality were increased in DN-NPRA as compared to WT-NPRA mice. In addition to their hormonal effects, endogenous natriuretic peptides exert physiologically relevant autocrine and paracrine effects via cardiomyocyte NPRA receptors to modulate cardiac hypertrophy and fibrosis in response to pressure overload.




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