Ventricular expression of brain natriuretic peptide in hypertrophic cardiomyopathy.

Abstract

These findings suggest that BNP is expressed in the ventricular myocytes of HCM with normal systolic function. In HOCM, ventricular expression of BNP may be augmented in response to both obstruction and diastolic dysfunction.

Doxorubicin Selectively Inhibits Brain Versus Atrial Natriuretic Peptide Gene Expression in Cultured Neonatal Rat Myocytes

“…12 They are both activated by similar provocative stimuli, typically those associated with cardiac hypertrophy. [13][14][15][16] They encode peptides that bind and activate the same receptor in target tissues at the periphery, and they display very similar physiological properties in laboratory animals and humans. Despite these similarities, the sensitivity of BNP gene expression to doxorubicin inhibition is much greater than that seen with ANP.…”

Molecular genetics of familial hypertrophic cardiomyopathy (FHC)

“…Calciumcalmodulin activated phosphatase-Calcineurin has been implicated in playing a major role in cardiac hypertrophy (Wilkins and Molkentin 2002). Several other growth factors, such as c-fos, c-jun, atrial and brain natriuretic peptides, and endothelin I, have been shown to be possibly involved in not only pressure overload hypertrophy but also in hypertrophy resulting from sarcomere gene mutations (Kai et al 1998;Derchi et al 1992;Hasegawa et al 1993Hasegawa et al , 1996. Adult cardiomyocytes in FHC have been shown to reactivate fetal isoforms and to down-regulate adult forms of several cardiac genes, including the cardiac myosin heavy chain gene (Komuro et al 1988;Chien et al 1993).…”

The Effect of Percutaneous Balloon Mitral Valvuloplasty on N-Terminal- Pro B- Type Natriuretic Peptide Plasma Levels in Mitral Stenosis

“…3,4) The N-terminal part of preproBNP (NT-proBNP) is secreted in a proportion equivalent to BNP and it was thought to be more sensitive because of its longer half-life. 5) Both BNP and NT-proBNP are synthesized and secreted by cardiac myocytes in response to volume expansion and pressure overload 1,6,7) and they also correlate with left ventricular filling pressures in patients with depressed systolic functions.…”