Chronic nicotine treatment enhances the depressor responses to arachidonic acid in the rat.

The depressor responses to intravenous injections of arachidonic acid, prostacyclin (PGI2), prostaglandin E2 (PGE2) and sodium nitroprusside were studied in chronically nicotine-treated rats. Arachidonic acid, PGI2, PGE2 and sodium nitroprusside decreased the diastolic blood pressure dose-dependently in the control animals. The vasodepressor effect of arachidonic acid was significantly enhanced in rats given nicotine 5 and 25 micrograms/ml in their drinking water for 10 days but remained unchanged in the animals treated with 1 microgram/ml nicotine for 10 days or given 1 mg/kg i.v. nicotine 10 min before administration of arachidonic acid. Indometacin abolished arachidonic-acid-induced depressor responses in both the control and nicotine-treated rats. Hypotension induced by PGI2, PGE2 and sodium nitroprusside was of similar magnitude in the control and nicotine-treated animals. It is suggested that the enhancement by chronic nicotine treatment of depressor responses to arachidonic acid could be due to changes in the formation and/or removal of its vaso-active metabolites (i.e. prostacyclin and/or thromboxane A2).