Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction

R. E. Mendez, J. M. Pfeffer, F. V. Ortola, K. D. Bloch, Sharon Anderson, J. G. Seidman, B. M. Brenner

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Abstract

To study the role of atrial natriuretic peptide (ANP) in chronic heart failure, ANP synthesis, storage, and release were examined by measuring atrial ANP messenger ribonucleic acid (mRNA) levels and atrial and plasma ANP concentrations in rats with myocardial infarction produced by coronary artery ligation. Three groups were defined as the following: 1) controls, sham-operated, or operated, but noninfarcted; 2) moderate infarcts, involving 5-30% of the left ventricular circumference; and 3) large infarcts (≥30%). In addition, to determine a possible modulation by dietary Na intake on ANP levels in heart failure, plasma immunoreactive ANP (iANP) levels were measured in rats with and without infarcts given low, regular, or high Na intake for 2 wk, by which time all groups were in neutral Na balance. Plasma iANP levels varied directly with increasing infarct and atrial sizes, irrespective of Na intake. In contrast, atrial ANP concentration varied inversely with increasing infarct size. The ANP mRNA content index, a measure of total atrial ANP mRNA, was significantly increased in rats with large infarcts compared with control rats. These results indicate that in rats with myocardial infarction, the severity of left ventricular dysfunction, as inferred from infarct size, but not chronic Na intake, is the primary determinant of the extent of activation of the ANP system. Elevated circulating ANP levels are maintained through enhanced atrial synthesis and release. ANP may thus play an important role in the hemodynamic and renal adaptations to chronic heart failure.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume253
Issue number6
StatePublished - 1987
Externally publishedYes

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Atrial Natriuretic Factor
Myocardial Infarction
Heart Failure
RNA
Left Ventricular Dysfunction
Ligation
Coronary Vessels
Hemodynamics

ASJC Scopus subject areas

  • Physiology

Cite this

Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction. / Mendez, R. E.; Pfeffer, J. M.; Ortola, F. V.; Bloch, K. D.; Anderson, Sharon; Seidman, J. G.; Brenner, B. M.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 253, No. 6, 1987.

Research output: Contribution to journalArticle

Mendez, R. E. ; Pfeffer, J. M. ; Ortola, F. V. ; Bloch, K. D. ; Anderson, Sharon ; Seidman, J. G. ; Brenner, B. M. / Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction. In: American Journal of Physiology - Heart and Circulatory Physiology. 1987 ; Vol. 253, No. 6.
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abstract = "To study the role of atrial natriuretic peptide (ANP) in chronic heart failure, ANP synthesis, storage, and release were examined by measuring atrial ANP messenger ribonucleic acid (mRNA) levels and atrial and plasma ANP concentrations in rats with myocardial infarction produced by coronary artery ligation. Three groups were defined as the following: 1) controls, sham-operated, or operated, but noninfarcted; 2) moderate infarcts, involving 5-30{\%} of the left ventricular circumference; and 3) large infarcts (≥30{\%}). In addition, to determine a possible modulation by dietary Na intake on ANP levels in heart failure, plasma immunoreactive ANP (iANP) levels were measured in rats with and without infarcts given low, regular, or high Na intake for 2 wk, by which time all groups were in neutral Na balance. Plasma iANP levels varied directly with increasing infarct and atrial sizes, irrespective of Na intake. In contrast, atrial ANP concentration varied inversely with increasing infarct size. The ANP mRNA content index, a measure of total atrial ANP mRNA, was significantly increased in rats with large infarcts compared with control rats. These results indicate that in rats with myocardial infarction, the severity of left ventricular dysfunction, as inferred from infarct size, but not chronic Na intake, is the primary determinant of the extent of activation of the ANP system. Elevated circulating ANP levels are maintained through enhanced atrial synthesis and release. ANP may thus play an important role in the hemodynamic and renal adaptations to chronic heart failure.",
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