α1-adrenergic stimulation induced hypertrophy in protein kinase C down-regulated cultured cardiac myocytes

被引：1

作者：

Kondo, H

Horiuchi, M

Hama, J

Kurooka, A

Shimada, S

Kamoi, K

Yamamoto, Y

Watanabe, M

Hidaka, H

Katori, R

Ishikawa, K

机构：

[1] Kinki Univ, Sch Med, Dept Internal Med 1, Osaka 5890041, Japan

[2] Nagoya Univ, Sch Med, Dept Pharmacol, Showa Ku, Nagoya, Aichi 4660000, Japan

来源：

CLINICAL AND EXPERIMENTAL HYPERTENSION | 1999年 / 21卷 / 03期

关键词：

cardiac myocyte; alpha(1)-adrenergic stimulation; cardiac hypertrophy; protein kinase C (PKC); phenylephrine; 12-tetra decanoylphorbol-13-acetate (TPA); down-regulation;

D O I：

10.3109/10641969909068664

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

To examine whether protein kinase C (PKC) activation is essential for the induction of cardiac myocyte hypertrophy caused by alpha(1)-adrenergic stimulation, we investigated the hypertrophic effect of phenylephrine in PKC down-regulated and non-treated cultured cardiac myocytes obtained from neonatal Sprague-Dawley rat ventricles. The treatment with 10 nmol/L 12-tetra decanoylphorbol-13-acetate (TPA) for more than 2 hours decreased PKC activity by approximately 80% without marked hypertrophy. Phenylephrine increased [C-14] phenylalanine (Phe) incorporation in both TPA non-treated and treated cells, 1.54- and 1.71-fold as large as control, respectively. The cell surface area also enlarged in both groups, 1.67- and 1.74-fold, respectively. Thus, phenylephrine induced the similar grade hypertrophy in cultured cardiac myocytes even when PKC was down-regulated. These results suggest that conventional PKC activation may not be essential for mediating myocyte hypertrophy by alpha(1)-adrenergic stimulation.

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收藏

页码：233 / 247

页数：15

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