1. The effect of isoprenaline (10 microM at 37 degrees C for 30 min) pretreatment on [125I]-(-)-pindolol ([125I]-(-)-Pin) binding to beta 2-adrenoceptors on intact human platelets has been examined. 2. By use of saturation analysis, maximal binding capacity (Bmax) of [125I]-(-)-Pin binding in control and treated cells was assessed in the presence of 1 microM (-)-propranolol or 1 microM (+/-)-CGP 12177 which were taken to represent total or cell surface beta-adrenoceptors respectively. Assay incubations were performed at 37 degrees C and 4 degrees C, the latter to prevent recycling of internalised receptors. 3. Isoprenaline treatment resulted in an identical, highly significant, loss of binding sites (approximately equal to 25%) defined by (-)-propranolol at both assay temperatures as compared to control cells. Binding sites identified in the presence of (+/-)-CGP 12177 were reduced to a much greater extent (approximately equal to 70%), but this was only seen when assays were performed at 4 degrees C. 4. Agonist-induced changes in receptor numbers were concentration-dependent with half maximal receptor loss occurring at an isoprenaline concentration of approximately 2 x 10(-8) M. These effects were inhibited by the presence of a beta-adrenoceptor antagonist and absent if agonist pretreatment was performed at 4 degrees C. 5. Recovery experiments showed that the isoprenaline-induced reduction in total receptor number defined by (-)-propranolol was irreversible whereas the reduction in cell surface receptors defined by (+/-)-CGP 12177 was rapidly reversible (less than 40 min). 6. These data suggest that isoprenaline treatment of intact human platelets causes redistribution of beta 2-adrenoceptors. A proportion are sequestered away from the cell surface (internalised), becoming inaccessible to the hydrophilic ligand (+/-)-CGP 12177. A smaller proportion defined by (-)-propranolol are apparently totally lost from the cell (down regulated).