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Correction for Poulos et al., Cardiovasc Res 55 (2) 238.
Cardiovascular Research 1996 32(5):909-919; doi:10.1016/S0008-6363(96)00138-1
© 1996 by European Society of Cardiology
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Copyright © 1996, European Society of Cardiology

Congestive heart failure: increased cardiac and extracardiac atrial natriuretic peptide gene expression

John E. Poulosa,b,1, William R. Gower, Jr.a,b, J.Thompson Sullebargera,b, Hector L. Fontaneta,b and David L. Vesely*,a,b

aDepartments of Biochemistry and Molecular Biology, Internal Medicine, Physiology and Biophysics, James A. Haley Veterans Hospital Tampa, FL 33612, USA
bUniversity of South Florida Health Sciences Center, Tampa FL 33612, USA

* Corresponding author, at: J.A. Haley Veterans Hospital-151, 13000 Bruce B. Downs Blvd., Tampa, FL 33612, USA. Tel. (+1-813) 972 7624; Fax (+1-813) 972 7623.

Objectives: The present investigation was designed to determine if atrial natriuretic peptide (ANP) gene expression increases in extracardiac as well as within the heart in congestive heart failure. Methods: Congestive heart failure (CHF) was induced by producing cardiac hypertrophy secondary to an aortocaval fistula in Sprague-Dawley rats. To characterize this model, control and CHF rats had cardiac catheterizations and transthoracic echocardiography. ANP messenger RNA was measured by RNAase protection analysis in atria, ventricles, liver, colon, and stomach of CHF and sham rats and quantitated by 2-D scanning. The product of ANP gene expression was determined in each of these tissues with high performance-gel permeation chromatography. To help determine if increased degradation of atrial natriuretic peptides occur in congestive heart failure, the circulating concentrations and the excretion of the atrial natriuretic peptides into urine were measured by specific radioimmunoassays. Results: ANP steady-state mRNA increased 4.2 ± 0.05 and 4.3 ± 0.06-fold, respectively, in the antrum of the stomach and within the heart ventricle of CHF rats compared with age-matched sham rats. ANP gene expression was present but not increased in atria, liver, and gastrointestinal tract of the CHF rats. High-performance gel permeation chromatography revealed that the product of this ANP gene expression within the stomach and heart ventricle in CHF animals was the ANP prohormone. There was not any decrease in the metabolism of these peptides; by the kidney in CHF. Conclusions: ANP steady-state mRNA increases in extracardiac (i.e., stomach antrum) tissue as well as in the ventricle of the heart in CHF. The product of the ANP gene expression, i.e., the ANP prohormone is the same in the extracardiac tissues as within the heart. Whether the increased extracardiac ANP steady-state mRNA and its resultant increased atrial natriuretic peptides helps prevent bowel wall edema in CHF needs to be elucidated.

KEYWORDS Atrial natriuretic factor; Gene expression; Heart failure; Rat, A-V fistular model

1 Present address: St. Louis Medical Center, 3635 Vista Ave. at Grand Blvd., P.O. Box 15250, St. Louis, MO 63110-0250, USA.


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Congestive heart failure: increased cardiac and extracardiac atrial natriuretic peptide gene expression
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