1. We previously demonstrated that
brain natriuretic peptide (BNP) is a cardiac
hormone mainly produced in the ventricle, while the major production site of
atrial natriuretic peptide (
ANP) is the atrium. The production and secretion of BNP and
ANP in the hypertrophied ventricles were markedly augmented, serving as a compensation mechanism against ventricular overload by their natriuretic,
diuretic and vasodilatory actions. 2. In the present study, we prepared an in vitro model of cardiocyte
hypertrophy using cultured neonatal rat ventricular cardiocytes and alpha1-adrenergic stimulation, and examined the gene expressions of BNP and
ANP during the process of cardiocyte
hypertrophy. 3. The treatment of cultured ventricular cardiocytes with
phenylephrine evoked cardiocyte
hypertrophy around 24 h after the treatment, which was characterized by augmented expression of the
myosin light chain-2 gene and increase in cell size. 4. In this model of cardiocyte
hypertrophy, the steady-state level of BNP
mRNA rapidly increased to the maximal level within 1 h after the treatment. In contrast,
ANP mRNA began to increase at 3 h, and accumulated during the course of cardiocyte
hypertrophy. The secretion of BNP from ventricular cardiocytes was also stimulated more rapidly than the
ANP secretion. 5. These results indicate that the gene expression of BNP is distinctly regulated from that of
ANP in cardiocyte
hypertrophy, and suggest a discrete pathophysiological role of BNP as an 'emergency' cardiac
hormone against ventricular overload.