1 The effects of the a2-adrenoceptor agonists clonidine, rilmenidine, TL99 and UK14304 on the vasoconstrictor response to sympathetic nerve stimulation and on the concentration-response curves to noradrenaline and phenylephrine were compared in two isolated, perfused vascular tissues: the rat tail artery (which has both postjunctional al-and a2-adrenoceptors), and the rabbit ear artery (in which only cx-adrenoceptors are present postjunctionally). 2 In the rabbit ear artery, the first observable effect of a2-adrenoceptor agonists was inhibition of vasoconstrictor responses to sympathetic nerve stimulation. This occurred with concentrations of the M2-adrenoceptor agonists which were far below those producing vasoconstriction. Responses to noradrenaline were not affected. 3 In contrast, in the rat isolated perfused tail artery, a2-adrenoceptor agonists, in concentrations that produced no other observable effects, enhanced the vasoconstrictor responses to sympathetic nerve stimulation and to noradrenaline. Much higher concentrations of a2-adrenoceptor agonists produced vasoconstriction in most preparations and only then reduced the response to sympathetic nerve stimulation. The enhancing effect of CX2-adrenoceptor agonists was blocked by idazoxan, but not by prazosin.4 Vasoconstrictor responses in the rat tail artery to the relatively selective xl-adrenoceptor agonist phenylephrine were enhanced by X2-adrenoceptor agonists. The enhancement of the response to phenylephrine was greater than that to the mixed a1-and a2-adrenoceptor agonist noradrenaline. 5 Vasoconstrictor responses in the rat tail artery to vasopressin, ATP and KCl, like those to a1-adrenoceptor agonists, were enhanced by a2-adrenoceptor agonists. However, vasoconstrictor responses to 5-hydroxytryptamine and angiotensin II were not enhanced.