Angiotensin II-induced hypertrophy of adult rat cardiomyocytes is blocked by nitric oxide

Rebecca H. Ritchie, Rick J. Schiebinger, Margot C. Lapointe, James D. Marsh

Research output: Contribution to journalArticleResearchpeer-review

108 Citations (Scopus)

Abstract

The aim of the present study was to test the hypothesis that bradykinin- stimulated release of nitric oxide (NO) and/or prostacyclin from endothelium blocks myocyte hypertrophy in vitro. Angiotensin II increased [3H]phenylalanine incorporation by 21 ± 2% in myocytes cocultured with endothelial cells; this was abolished by bradykinin in the presence of endothelial cells. Bradykinin increased cytosolic concentrations of cGMP by 29 ± 4% in myocytes cocultured with endothelial cells. This was abolished by inhibition of NO synthase and by a cyclooxygenase inhibitor. Angiotensin II also increased [3H]phenylalanine incorporation by 28 ± 3% in myocytes cultured in the absence of endothelial cells. This effect of angiotensin II in monoculture was abolished by donors of NO but not by bradykinin. Neither the stable analog of prostacyclin (iloprost) nor the prostacyclin second messanger analog 8-bromo-cAMP (8-BrcAMP) blocked the effect of angiotensin II. Furthermore, 8-BrcAMP and iloprost individually increased [3H]phenylalanine incorporation. The anti-hypertrophic effects of bradykinin are critically dependent on endothelium-derived NO.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume275
Issue number4 44-4
Publication statusPublished - 9 Nov 1998
Externally publishedYes

Keywords

  • Angiotensin converting-enzyme inhibitors
  • Bradykinin
  • Endothelium
  • Prostacyclin

Cite this