Serotonin and Raynaud's phenomenon.

No single pathophysiologic mechanism explains adequately cold-induced vasospasm in all forms of Raynaud's phenomenon. Local serotonin release from activated platelets is a contributory element in those disorders typified by structural arterial change, e.g., systemic sclerosis (scleroderma). Selective antagonism of S2-serotonergic receptors with ketanserin improves both maximal digital artery flow and cold tolerance. Platelet-derived growth factors, and serotonin itself, may contribute to the fibrotic arteriosclerosis of this disorder. In contrast, in primary (spastic) Raynaud's phenomenon, ketanserin relieves but does not prevent cold-induced vasospasm, which suggests that the role of serotonin is in maintenance of but not provocation of an attack. Antiplatelet therapies could benefit both disorders.