[Role of the endothelium in the function of vascular fibers]

J Pharmacol. 1983:14 Suppl 3:73-9.
[Article in French]

Abstract

The endothelial cells can enzymatically activate (e.g. angiotensin II) or destroy (e.g. bradykinin, norepinephrine, 5-hydroxytryptamine) vasoactive substances present in the blood (fig. 1). They also generate prostacyclin, which in several vascular areas has potent vasodilator properties (fig. 1). In addition, endothelial cells play an obligatory role in the relaxation induced by acetylcholine in isolated arteries (fig. 2). This is also the case for the inhibitory effect of adenosine triphosphate (fig. 3), arachidonic acid, bradykinin, histamine and thrombin. The inhibitory responses generated by the endothelial cells are not all mediated by identical cellular events. Thus, the endothelium-mediated relaxations induced by arachidonic acid are due mainly to the production of prostacyclin, while those induced by acetylcholine, bradykinin and histamine involve a product of lipoxygenase; the mechanism underlying endothelium-mediated responses to adenosine triphosphate and thrombin are unknown (fig. 4). In isolated veins contracted with norepinephrine, thrombin and arachidonic acid cause increases in tension which are abolished by endothelium removal. In several arteries and veins, the absence of endothelium prevents or reduces the occurrence of further contractions caused by anoxia. Thus, the cells of the intima recognize the presence of certain substances in the blood and in turn generate signals which alter the contractile behavior of the smooth muscle cells of the media.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Acetylcholine / physiology
  • Animals
  • Biogenic Amines / physiology
  • Endothelium / metabolism
  • Endothelium / physiology
  • Humans
  • In Vitro Techniques
  • Muscle, Smooth, Vascular / physiology*
  • Vasoconstriction
  • Vasodilation

Substances

  • Biogenic Amines
  • Acetylcholine