alpha 2-Adrenoceptor agonists cause both mydriasis and platelet aggregation. This work is aimed at identifying the factors accompanying and affecting mydriatic activity. For eight imidazol(in)e drugs mydriatic, hypotensive and bradycardic activities were determined in rats. The lipophilicity of the agents was determined chromatographically and calculated theoretically. A correlation was found between the hypotensive and the bradycardic potency and between the mydriatic activity and both the hypotensive and bradycardic activity. Mydriatic activity depended on the lipophilicity of the agents studied. The human platelet antiaggregatory activity of the drugs did not correlate with either the mydriatic or cardiovascular activity and it was independent of lipophilicity. The dependence of the centrally induced effects on lipophilicity and the lack of such a dependence in the case of the in vitro alpha 2-adrenoceptor-mediated platelet aggregation may be interpreted as resulting from heterogeneity of the rat cerebral and the human platelet alpha 2-adrenoceptors. The alpha 2-adrenergic activity of drugs in the model of mydriasis in rats cannot be predicted from their activity in causing human platelet aggregation in vitro.