Platelets differ from other formed elements of blood in expressing mechanisms for uptake, storage, and endocytotic release of 5-HT. 5-HT is not synthesized in platelets, but is taken up from the circulation and stored in secretory granules by active transport, similar to the uptake and storage of NE by sympathetic nerve terminals (see Chapters 6 and 12). Measuring the rate of Na+-dependent 5-HT uptake by platelets provides a sensitive assay for 5-HT-uptake inhibitors.
A complex local interplay of multiple factors, including 5-HT, regulates thrombosis and hemo-stasis (see Chapters 25 and 54). When platelets contact injured endothelium, they release substances that promote platelet aggregation, and secondarily, they release 5-HT (Figure 11-3). 5-HT binds to platelet 5-HT2A receptors and elicits a weak aggregation response that is markedly augmented by the presence of collagen. If the damaged blood vessel is injured to a depth where vascular smooth muscle is exposed, 5-HT exerts a direct vasoconstrictor effect, thereby contributing to hemostasis, which is enhanced by locally released autocoids (thromboxane A2, kinins, and vasoactive peptides). Conversely, 5-HT may stimulate production of NO and antagonize its own vasoconstrictor action, as well as the vasoconstriction produced by other locally released agents.
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