The main action of adenosine on vascular beds is vasodilation via A(2) rece
ptors. In addition, A(1) receptors are found in some blood vessels, where t
hey cause contraction. Traditionally, adenosine-induced vasodilation in vit
ro has been attributed to A(2A) receptor activation; however, it is now cle
ar that A(2B) receptors are also involved in the regulation of vascular ton
e. Endothelium dependence of A(2) receptor-mediated responses is variable;
in some tissues they are blocked by removal of endothelium and/or inhibitio
n of NO-synthase and in some they are not. In addition to A(2) receptor-med
iated relaxation, there is much evidence that relaxations to adenosine and
some of its analogues can also be mediated by a mechanism which cannot be b
locked by adenosine receptor antagonists. There is evidence that these resp
onses 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 sign
ificance. Drug Dev. Res. 52:346-349, 2001. (C) 2001 Wiley-Liss, Inc.