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.
J R
JR
Seibold
D001792:Blood Platelets / Q000502:physiology; D006801:Humans; D010991:Plethysmography; D011928:Raynaud Disease / Q000503:physiopathology*; D012039:Regional Blood Flow; D012595:Scleroderma, Systemic / Q000503:physiopathology; D012701:Serotonin / Q000502:physiology*
D012701:Serotonin