TY - JOUR
T1 - GENE REGULATION OF BRAIN NATRIURETIC PEPTIDE IN CARDIOCYTE HYPERTROPHY BY α1‐ADRENERGIC STIMULATION
AU - Nakagawa, O.
AU - Itoh, H.
AU - Harada, M.
AU - Komatsu, Y.
AU - Yoshimasa, T.
AU - Nakao, K.
PY - 1995/11
Y1 - 1995/11
N2 - 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 αl‐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 3h, 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.
AB - 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 αl‐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 3h, 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.
KW - atrial natriuretic peptide
KW - brain natriuretic peptide
KW - cardiac hypertrophy
KW - gene expression
KW - ventricular cardiocytes
KW - α ‐adrenergic receptor
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U2 - 10.1111/j.1440-1681.1995.tb02873.x
DO - 10.1111/j.1440-1681.1995.tb02873.x
M3 - Article
C2 - 9072347
AN - SCOPUS:0029558515
SN - 0305-1870
VL - 22
SP - S183-S185
JO - Clinical and Experimental Pharmacology and Physiology
JF - Clinical and Experimental Pharmacology and Physiology
ER -