Inhibition of moderate hypoxia-induced protein synthesis by vasonatrin peptide in cultured neonatal rat cardiomyocytes.
- Author:
Shun-Yan LU
1
;
Miao-Zhang ZHU
;
Hai-Tao GUO
;
Jun YU
;
Qi-Ming WEI
Author Information
1. Department of Physiology, The Fourth Military Medical University, Xi an 710032 mz_zhu@fmmu.edu.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Atrial Natriuretic Factor;
pharmacology;
Cell Hypoxia;
Cells, Cultured;
Cyclic AMP;
metabolism;
Cyclic GMP;
metabolism;
Dose-Response Relationship, Drug;
Endothelins;
biosynthesis;
Myocytes, Cardiac;
metabolism;
Protein Biosynthesis;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2002;54(1):7-11
- CountryChina
- Language:Chinese
-
Abstract:
The present work was to investigate the effects of vasonatrin peptide (VNP) on cardiomyocyte protein synthesis induced by moderate hypoxia. In cultured neonatal rat cardiomyocytes, MTT methods, total protein measurement and (3)H-leucine incorporation were used to calculate the cell number and measure the protein synthesis of cardiomyocytes. Furthermore, radioimmunoassay was undertaken to observe the effects of VNP on the intracellular levels of cAMP, cGMP and the concentration of endothelin (ET) in the culture medium. The results showed that both the cell number and protein synthesis decreased with severe hypoxia for 24 h. In contrast, under moderate hypoxia, cardiomyocyte hypertrophy developed; the protein synthesis as evidenced by total protein content and 3H-eucine incorporation increased significantly. VNP reduced cardiomyocyte protein synthesis induced by moderate hypoxia in a dose-dependent manner. Furthermore, VNP increased the intracellular level of cGMP and decreased the concentration of ET in the culture medium under moderate hypoxia, but had no effect on the level of cAMP. These results suggest that VNP inhibits moderate hypoxia-induced protein synthesis in cultured neonatal rat cardiac myocytes. This effect is mediated, at least in part, by an increase in intracellular cGMP, a reduction in synthesis, and/or a release in ET of cardiomyocytes.
