ABSTRACT
Endothelium-dependent relaxations have been demonstrated in isolated conduit arteries, and also in resistance vessels, of most mammalian species including humans, with a variety of agonists. Mechanical removal of the endothelium, laser-induced endothelial injury, air embolism, or inhibitors of endothelium-derived relaxing factor (EDRF) reduces or abolish the vasodilatation induced by acetylcholine or carbachol in the intact organism. Endothelial communication could be achieved by cell-to-cell contact, particularly at the microcirculatory level where close connections exist between endothelial cells and vascular smooth muscle. However, in large blood vessels, the release of an EDRF has been confirmed with cascade-bioassay techniques using either perfused blood vessels with endothelium or microcarrier beads covered with cultured endothelial cells as donor tissues. The relaxation induced by acetylcholine cannot be attributed to the release of prostaglandins or adenosine. Indeed, inhibitors of cyclooxygenase and purinergic antagonists, respectively, do not affect the relaxation induced by the muscarinic agonist.
