1. The effect of indomethacin, an inhibitor of prostaglandin synthesis, on number and sensitivity of α- and β-adrenoreceptors was studied in normal healthy volunteer subjects. 2. The subjects were studied under metabolic conditions. To achieve inhibition of prostaglandin synthesis indomethacin (2 mg day −1 kg −1 ) was given orally for 7 days. This dose decreased urinary excretion of prostaglandin E-like immunoreactivity by 70%. 3. The number of α-adrenoreceptors was measured by the specific binding of [ 3 H]dihydroergocryptine to platelet membranes and that of β-adrenoreceptors by the binding of [ 3 H]dihydroalprenolol to leucocyte membranes. 4. The number of α-adrenoreceptors did not change with indomethacin, nor did basal, prostaglandin E 1 - or noradrenaline-stimulated cyclic AMP production by platelet membranes. In contrast, the number of β-adrenoreceptors increased by 92%. Indomethacin did not affect, however, basal, 1-isoprenaline- or prostaglandin E 1 -stimulated cyclic AMP production in leucocyte membranes. 5. These results suggest that a reflex-mediated decrease in sympathetic discharge in response to an indomethacin-induced decrease in release of vasodilator prostaglandins may lead to an ‘up-regulation’ of β-adrenoreceptor sites.