Previous studies have shown that abnormalities in collagen-induced platelet aggregation may be due to an impaired release of storage pool ADP, the agent ultimately responsible for platelet aggregation. In some patients and in normal subjects who ingest aspirin, the storage pool of ADP is present in normal amounts, but the mechanism for releasing it appears to be defective ("aspirin-like" defect). In these subjects, the centripetal reorientation of the platelet granules, which may be early structural changes of the release reaction, failed to occur. In one preleukemic patient with an aspirin-like defect, the elements of the open-channel system were also increased. In a second group of patients the impairment of aggregation is due to a deficiency of storage pool ADP. In these patients with storage pool disease, the initial ultrastructural changes associated with the collagen-induced release reaction were normal. The most striking abnormality was a marked decrease in the number of platelet dense bodies. Since the platelets of these patients are deficient in both serotonin and the storage pool of adenine nucleotides, the findings suggest that, in human platelets, these substances are normally stored in the dense bodies. A defect in the formation or function of the dense bodies may account for the abnormalities of platelet aggregation in storage pool disease.