Effects of pyridine and some of its derivatives on prostaglandin synthesis

Effects of pyridine and some of its derivatives namely, nicotinic acid, nicotinyl alcohol, pyridinol carbamate, pyridoxine hydrochloride and pyridostigmine bromide were investigated on the release of a prostaglandin E2-like substance (PGE2-LS) from the isolated perfused rat heart. Furthermore, the effect of neostigmine bromide was also studied as a non-pyridine control compound. At 2 X 10(-5) M concentration, only pyridoxine hydrochloride stimulated the release of PGE2-LS significantly. At 2 X 10(-4) M concentration, pyridine, nicotinic acid and pyridinol carbamate were also found to be active in addition to pyridoxine hydrochloride. At 1 X 10(-3) M concentration, pyridine and all of its derivatives studied increased the release of PGE2-LS significantly. However, neostigmine bromide (1 X 10(-3) M) failed to exert any effect. Indomethacin, a prostaglandin synthetase inhibitor, reduced both the basal release (28%) and the release stimulated by pyridine and its derivatives at 1 X 10(-3) M concentration (more than 50%). These findings suggest that the active substance released is a prostaglandin. It is concluded that the PGE2-LS releasing effect of pyridine and its derivatives from isolated rat heart may be due to the action of the pyridine moiety of the molecules of the compounds studied.