Interaction of rilmenidine and clonidine with pre- and postjunctional alpha-adrenoceptors in rat and rabbit blood vessels and in rat kidneys.

In several blood vessels, the influence of the alpha 2-adrenoceptor agonists rilmenidine and clonidine was compared. In aortas of rat and rabbit and in the rabbit pulmonary artery, both compounds evoked contractions due to stimulation of postjunctional alpha 1-adrenoceptors. In the aorta of the rat, but not in that of the rabbit, removal of the endothelium markedly enhanced the contractions to rilmenidine and clonidine. At the alpha 1-adrenoceptors, clonidine was about 135 times more potent than rilmenidine. The activity of both substances at post- and prejunctional alpha 2-adrenoceptors was compared in the rabbit saphenous vein. Rilmenidine and clonidine evoked contractions of the vein by stimulating postjunctional alpha 2-adrenoceptors and decreased the stimulation-induced overflow of [3H]-noradrenaline by activating the prejunctional alpha 2-adrenoceptors. At the post- and prejunctional alpha 2-adrenoceptors, clonidine was about 30 times more potent than rilmenidine. These data illustrate that, although less potent than clonidine, rilmenidine is 5 times more specific for the alpha 2-adrenoceptors. In the isolated perfused rat kidney, rilmenidine and clonidine antagonized the vasoconstrictions induced by noradrenaline. Although the exact mechanism of this inhibitory response remains to be elucidated, our results indicate that rilmenidine may possess some interesting properties at the level of the renal circulation.