Methylnicotinate stimulated prostaglandin synthesis in patients with schizophrenia: A preliminary investigation.

Schizophrenia is a serious mental illness of unclear aetiology. The reduced ability of methylnicotinate to induce a topical vasodilatory response in patients with the disorder is well established. Methylnicotinate causes vasodilation via stimulating the release of prostaglandins (including prostaglandin D2 ) in the skin which in turn leads to relaxation of vascular smooth muscle. To determine whether the abnormality is likely to be due to decreased prostaglandin production, or a decreased effect of prostaglandins upon the vessels, topical methylnicotinate was applied to the forearms of patients with schizophrenia or healthy controls, followed by rating of the resulting erythema. The concentration of prostaglandin D2 and its metabolite 11β-prostaglandin F2α in the blood draining the arm was also measured. Although erythema was reduced in the patient group, this was not correlated with plasma prostaglandin concentrations. This data suggests the abnormality underlying the reduced potency of methylnicotinate to produce vasodilation in the disorder occurs downstream of prostaglandin synthesis possibly within the vasculature itself.