Vascular effects of adenosine and its analogues

Abstract

AbstractThe main action of adenosine on vascular beds is vasodilation via A2 receptors. In addition, A1 receptors are found in some blood vessels, where they cause contraction. Traditionally, adenosine‐induced vasodilation in vitro has been attributed to A2A receptor activation; however, it is now clear that A2B receptors are also involved in the regulation of vascular tone. Endothelium dependence of A2 receptor‐mediated responses is variable; in some tissues they are blocked by removal of endothelium and/or inhibition of NO‐synthase and in some they are not. In addition to A2 receptor‐mediated relaxation, there is much evidence that relaxations to adenosine and some of its analogues can also be mediated by a mechanism which cannot be blocked by adenosine receptor antagonists. There is evidence that these responses are endothelium‐ and NO‐independent and that, under conditions where adenosine is taken up into cells, relaxations to the endogenous ligand are entirely mediated by this mechanism, suggesting it is of physiological significance. Drug Dev. Res. 52:346–349, 2001. © 2001 Wiley‐Liss, Inc.