The role of chelation and of human plasma in the uptake of serotonin by human platelets.

Recent studies in this laboratory of platelets from patients with rheumatoid arthritis and nonrheumatoid inflammatory states (1) have emphasized the importance of the transport system or systems concerned with absorption and release of serotonin by platelets. There is no agreement or definite knowledge concerning such transport mechanisms at present. Born, Ingram and Stacey (2) reported a positive correlation between serotonin (5HT) absorption and ATP content in platelets, and Baker, Blaschko and Born (3) observed that 5HT and ATP were present in the same cytoplasmic fraction of platelets. Hughes, Shore and Brodie (4) felt that the rapid inhibition of uptake of serotonin produced by reserpine suggested blocking of an energetic transport mechanism for absorption, whereas the slow rate of release of serotonin from such platelets was consistent with passive diffusion. As regards an active absorption mechanism, Sano, Kakimoto and Taniguchi (5) noted a stimulatory effect of glucose on absorption of serotonin by rabbit platelets; they attributed this to ATP formed during glucose oxidation and suggested that ATP supplied the energy for absorption. However, inhibition of glucose metabolism did not result in slow release of serotonin as might have been expected with passive diffusion. An additional enzymatic mechanism for release was postulated therefore. Weissbach, Bogdanski and Udenfriend (6) and Weissbach, Redfield and Titus (7) called attention to the role of phosphates and potassium in the uptake of serotonin by saline suspensions of human platelets and to the inhibitory effect of cardiac glycosides on this system. They noted evidences for different mechanisms of uptake in different systems in vitro. In the present study the problem of uptake of 5HT was explored by two types of experiments.