Experiments were designed to study adrenoceptor function in subjects with Raynaud''s disease. Sympathetic agonists and antagonists were administered into the finger skin by iontophoresis, and the resulting change in local skin blood flow was evaluated by laser Doppler technique. The effects of norepinephrine (NE, stimulating .alpha.1- and .alpha.2-adrenoceptors), phenylephrine (stimulating .alpha.1-adrenoceptors), and B-HT 933 (stimulating .alpha.2-adrenoceptors) were studied in 12 women with Raynaud''s disease and in 12 healthy controls. Controls and cases showed a similar consistent vasoconstriction to NE and B-HT 933. All control subjects showed a vasoconstriction to phenylephrine. In contrast, the Raynaud subjects demonstrated a weaker vasoconstriction or even a vasodilation, especially to low concentrations of the drug. After blockade of the .alpha.1-adrenoceptors by doxazosin in the controls, phenylephrine mimicked the reaction in Raynaud subjects. .beta.-Adrenoceptor agonists (isoprenaline and terbutaline) had no effect on finger blood flow in the examined finger skin area in either control or Raynaud subjects. We suggest that Raynaud''s disease is characterized by a defect in .alpha.1-adrenoceptor function.