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Biochemical and physiological evidences for antiserotonergic properties of naftidrofuryl.

In experimental and clinical investigations, 2-(diethylamino)ethyl-tetrahydro-alpha-(1-naphthyl-methyl)-2-furanpro pionate (naftidrofuryl, Praxilene) appears to improve blood flow and microcirculation in ischemic areas. In order to define the mechanism by which the drug may exert its vascular effects, the binding affinity of naftidrofuryl toward various receptors was studied. From this biochemical study, it appeared that, in therapeutic doses, naftidrofuryl selectively inhibited the binding of spiperone or ketanserin to serotonin S2 receptors. This finding was corroborated in physiological models such as isolated rat caudal arteries or preparations of aortic myocytes. Naftidrofuryl effectively blocked the constrictive effect of serotonin on the artery in a dose-dependent, competitive manner. It also strongly inhibited the formation of serotonin-stimulated inositol triphosphate in the myocytes. From these good correlations between biochemical and physiological data it is concluded that the beneficial effects of naftidrofuryl on ischemic tissue perfusion may be partly explained on the basis of selective antiserotonergic S2 properties.