Atrial natriuretic peptide inhibits the expression of tissue factor and plasminogen activator inhibitor 1 induced by angiotensin II in cultured rat aortic endothelial cells

Thromb Haemost. 1998 Mar;79(3):631-4.

Abstract

The pharmacological characteristics of atrial natriuretic peptide (ANP), such as natriuresis, vasodilation, or suppression of smooth muscle cell proliferation, are well investigated. However, this is the first study to report its role on blood coagulation and fibrinolysis mediated by vascular endothelial cells. In this study, the effects of ANP on the enhanced expression of tissue factor (TF) and plasminogen activator inhibitor 1 (PAI-1) by angiotensin II (Ang II) in cultured rat aortic endothelial cells (RAECs) were examined. The expressions of TF and PAI-1 mRNA were detected by northern blotting methods. The activities of TF on the surface of RAECs and PAI-1 in the culture media were measured by chromogenic assay. ANP suppressed mRNA expressions of TF and PAI-1 induced by Ang II in a concentration-dependent manner. This suppression was accompanied by the decreased activities of TF and PAI-1.

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Atrial Natriuretic Factor / pharmacology*
  • Cells, Cultured
  • Drug Antagonism
  • Endothelium, Vascular / metabolism*
  • Male
  • Plasminogen Activator Inhibitor 1 / biosynthesis*
  • Rats
  • Rats, Sprague-Dawley
  • Thromboplastin / biosynthesis*
  • Vasoconstrictor Agents / pharmacology*

Substances

  • Plasminogen Activator Inhibitor 1
  • Vasoconstrictor Agents
  • Angiotensin II
  • Atrial Natriuretic Factor
  • Thromboplastin