An attempt has been made to classify the subtypes of alpha-adrenoreceptors mediating renal vasoconstriction in vivo using renal nerve stimulation and alpha-adrenoreceptor agonists and antagonists of varying selectivity in anesthetised rabbits. In the first series of experiments prazosin more potently inhibited the phenylephrine than the nerve induced renal vasoconstriction while phentolamine inhibited the response to phenylephrine and nerve stimulation nearly equally. In the second series of experiments low to moderate doses of yohimbine potently inhibited the renal vasoconstriction of clonidine, was less potent on that induced by noradrenaline and did not significantly affect that of phenylephrine. Prazosin was a potent antagonist of phenylephrine induced vasoconstriction but was less potent on nerve stimulation and noradrenaline, and was without effect on clonidine. In the third series of experiments, prazosin partially inhibited the renal vasoconstriction produced by all frequencies of nerve stimulation and that produced by high doses of noradrenaline. The prazosin resistant component of nerve stimulation and exogenous noradrenaline was significantly reduced by the addition of yohimbine. These results have been taken to suggest the presence of both alpha 1- and alpha 2-adrenoreceptors in the renal vasculature of the rabbit which mediate the renal vasoconstriction of exogenous and endogenous noradrenaline. They further show that in the rabbit the alpha 2-adrenoreceptors mediate a much greater proportion of the total renal vasoconstriction compared with the dog, cat or rat in which the alpha 1-adrenoreceptor population appears to be the predominant receptor.