[Effect of protein kinase C on inhibition of nitric oxide synthesis in cultured neonatal rat cardiomyocytes by angiotensin II]

Sheng Li Xue Bao. 2000 Aug;52(4):318-22.
[Article in Chinese]

Abstract

The purpose of the present study was to investigate the effect of angiotensin II (Ang II) on nitric oxide (NO) concentration and its signal transduction pathway in cultured neonatal rat cardioymocytes. NO content was measured in cultured neonatal rat cardiomyoctes using a nitrite/nitrate colormetric method kit. NO content was represented by measured nitrite (NO(2)) and nitrate (NO(3)) level (NO(2)/NO(3)). The results are as follows. NO production was decreased by Ang II in a dose dependent manner but increased by L Arg. The Saralasin, an antagonist of Ang II receptor, inhibited the effect of Ang II on NO production. The effect of Ang II on NO production was inhibited by NOS blocker N(G)-nitro-L-arginine methyl ester L-NAME but not by L-Arg. Pretreatment of Phorbol 12-myristate 13-acetate PMA , a PKC activator, decreased NO concentration significantly. This effect was strengthened by L-NAME. Staurosporine, a PKC inhibitor, abolished the inhibiting effect of Ang II on production of NO. The above results suggest that Ang II could decrease NO content in cultured neonatal rat cardiomyocytes significantly. Activity of NOS may be inhibited by Ang II. Ang II receptor was involved in the inhibitory effect of Ang II on NO production. Activation of protein kinase C (PKC) decreased significantly NO production in cultured neonatal rat cardiomyoctes, which appears to be associated with PKC in the signal transduction pathway.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Animals, Newborn
  • Cells, Cultured
  • Depression, Chemical
  • Female
  • Male
  • Myocytes, Cardiac / metabolism*
  • Nitric Oxide / biosynthesis*
  • Protein Kinase C / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction

Substances

  • Angiotensin II
  • Nitric Oxide
  • Protein Kinase C