B-type natriuretic peptide: a myocyte-specific marker for characterizing load-induced alterations in cardiac gene expression

Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and C-type natriuretic peptide are the known members of the mammalian natriuretic peptide system. ANP and BNP genes are expressed in a specific manner in cardiac myocytes. They are natriuretic and diuretic hormones and cause vasorela...

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Bibliographic Details
Published inAnnals of medicine (Helsinki) Vol. 30 Suppl 1; p. 39
Main Authors Magga, J, Vuolteenaho, O, Tokola, H, Marttila, M, Ruskoaho, H
Format Journal Article
LanguageEnglish
Published England 01.08.1998
Subjects
Adult
Animals
Cardiac Volume - physiology
Cells, Cultured
Child, Preschool
Dogs
Gene Expression
Genetic Markers - physiology
Guanylate Cyclase - genetics
Guanylate Cyclase - metabolism
Humans
Hypertrophy, Left Ventricular - physiopathology
Mice
Mice, Transgenic
Myocardium - cytology
Myocardium - metabolism
Rats
Receptors, Atrial Natriuretic Factor - genetics
Receptors, Atrial Natriuretic Factor - metabolism
Sensitivity and Specificity
Swine
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Summary:Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and C-type natriuretic peptide are the known members of the mammalian natriuretic peptide system. ANP and BNP genes are expressed in a specific manner in cardiac myocytes. They are natriuretic and diuretic hormones and cause vasorelaxation. ANP is mainly synthesized in the atria of the normal adult heart. However, ventricular hypertrophy is characterized by an augmentation of the synthesis and release of ANP from the ventricles. BNP is expressed in both the atria and the ventricles, but is mainly released from the ventricles. The major determinant of ANP and BNP secretion is wall stretch, and the levels of BNP messenger RNA increase substantially in response to cardiac overload. Acute increase in BNP gene expression occurs within 1 h and mimics the rapid induction of proto-oncogenes in response to haemodynamic stress. BNP can be used as a myocyte-specific marker to identify mechanisms that couple acute mechanical overload to alterations in cardiac gene expression.
ISSN:0785-3890