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

Prostaglandins Leukot Essent Fatty Acids. 2018 Sep;136:99-102. doi: 10.1016/j.plefa.2017.05.002. Epub 2017 May 19.

Abstract

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 F 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.

Keywords: Niacin; Prostaglandin; Schizophrenia; Vasodilation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Female
  • Humans
  • Male
  • Middle Aged
  • Nicotinic Acids / pharmacology*
  • Prostaglandin D2 / blood*
  • Schizophrenia / blood
  • Schizophrenia / metabolism*
  • Skin / drug effects
  • Vasodilator Agents / pharmacology*

Substances

  • Nicotinic Acids
  • Vasodilator Agents
  • methyl nicotinate
  • Prostaglandin D2