Influence of nitric oxide on the angiotensin II-activated protein kinase C activity in cultured neonatal rat cardiomycytes.
- Author:
Shi-Gan FU
1
;
Xie-Ju XIE
;
Li-Min JI
;
Pei-Qing LIU
;
Jing-Yun PAN
;
Wei LU
Author Information
1. Department of Physiology, Hainan Medical College, Haikou 571101. fushigan@yahoo.com.cn
- Publication Type:Journal Article
- MeSH:
Angiotensin II;
physiology;
Animals;
Animals, Newborn;
Cells, Cultured;
Female;
Male;
Myocytes, Cardiac;
cytology;
enzymology;
Nitric Oxide;
physiology;
Protein Kinase C;
metabolism;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2003;55(1):53-57
- CountryChina
- Language:Chinese
-
Abstract:
We examined the effect of endogenous and exogenous nitric oxide (NO) on protein kinase C (PKC) activity induced by angiotensin II (Ang II) in cultured neonatal rat cardiomyocytes. The results are as follows. The activity of PKC was increased by Ang II (0.01-10 micromol/L) in a dose-dependent manner, but decreased by NO precursor L-arginine (L-Arg) (10 micromol/L-10 mmol/L) in a dose-dependent manner in cultured neonatal rat cardiomyocytes. Pretreatment with L-Arg (100 micromol/L) decreased significantly Ang II -activated PKC activity and PKC activity induced by phorbol 12-myristate 13-acetate (PMA) ( 10 micromol/L), a PKC activator. Pretreatment with N(G)-nitro-L-argingie methyl ester (L-NAME), a nitric oxide synthase (NOS) blocker, may inhibit significantly the role of L-Arg on Ang II - and PMA-activated PKC activity. The activity of PKC was also decreased by NO donor sodium nitroprusside (SNP) (10 micromol/L-1 mmol/L) in a dose-dependent manner in cultured neonatal rat cardiomyocytes. Pretreatment with SNP (10 micromol/L) decreased significantly Ang II - and PMA-activated PKC activity. These results indicate that PKC was controlled by both NO and Ang II. PKC may be a cross talk between Ang II and NO in cardiomyocytes. NO abolished the activity of PKC and impaired PKC downstream signaling transduction pathway cascades.
