Serotonin and the peripheral circulation.

A recent resurgence of interest into the role of platelets in the pathogenesis of ischaemic syndromes associated with atherosclerosis, and the development of new antagonists for major platelet products, has led to a broad range of studies into the mechanisms by which serotonin, and other factors released by platelets, may contribute to ischaemia. Serotonin influences large arteries in vivo to induce constriction through an action on the 5-HT2 serotonin receptor. Several studies now show, at least for the limb blood supply, that collateral arteries after major artery occlusion are extremely sensitive to serotonin acting on the 5-HT2 serotonin receptor. Preliminary studies on platelet activation secondary to endothelial damage induced by mechanical abrasion in the rabbit with collateral limb vessels indicate that vasoactive quantities of serotonin are, indeed, released and that the response of the collateral vessels is reversed, at least in part, by ketanserin. Preliminary evidence also indicates that simultaneous blockade of serotonin and thromboxane achieves a greater effect than blocking either alone, following platelet activation.