Intra-arterial administration of (+)- and (-)-isomers of adrenaline and noradrenaline produced dose-related contraction of the nictitating membrane (NM) and dilation of the pupil in anesthetized cats. The relative potencies were (-)-adrenaline greater than (+)-adrenaline = (-)-noradrenaline greater than (+)-noradrenaline. Observations of the effects of alpha-adrenoceptor antagonists on (-)-noradrenaline activation of these two effectors were made simultaneously. All of the alpha 1-adrenoceptor antagonists tested produced a dose-related blockade of the NM with the relative potencies being prazosin greater than WB-4101 greater than phentolamine greater than phenoxybenzamine. In contrast, the iris dilator was blocked by WB-4101 and phenoxybenzamine but was refractory to antagonism by doses of prazosin and phentolamine that reduced the (-)-noradrenaline evoked NM response by 75-80% in the same animals. The alpha 2-adrenoceptor antagonist, yohimbine, produced significant inhibition of the NM only at high dose (1 mg/kg) but even at this level had no effect on pupil diameter. These results suggest that activation of the NM by exogenous noradrenaline is due solely to stimulation of alpha 1-adrenoceptors. alpha 2-adrenoceptors do not seem to significantly contribute to noradrenaline induced activation of either the NM or iris dilator muscle in vivo. In contrast, the alpha-adrenoceptors on the iris dilator muscle that are stimulated by exogenous noradrenaline can not easily be classified pharmacologically as either alpha 1- or alpha 2-adrenoceptors.