Endothelial adrenoceptors

alpha2 -Adrenergic agonists cause endothelium-dependent relaxation in a number of isolated blood vessels. This effect is explained by the activation of endothelial alpha 2 -adrenoceptors linked to nitric oxide synthase by G i -coupling proteins. The endothelial response to alpha 2 -adrenergic agonists is blunted considerably after regeneration of the endothelium and in atherosclerotic arteries. The relaxation of isolated arteries caused by beta-adrenergic agonists is reduced by removal of the endothelium and, in most cases, by inhibitors of the l -arginine nitric oxide pathway. Likewise, in the intact animal and in the human forearm the vasodilatation to beta 2 -adrenergic agonists is blunted by inhibitors of nitric oxide synthase. Whether these findings reflect the presence of functional beta-adrenoceptors on the endothelium remains controversial. Several beta-adrenergic blockers cause endothelium-dependent relaxation in vitro or augment the production of nitric oxide in vivo. However, these responses cannot be attributed to interactions with endothelial beta-adrenoceptors.