ABSTRACT
Influences of 2.5 and 5% (w/v) aqueous tea and coffee beverages administered ad lib. to rats for two weeks on PGI2 synthesis by the rat thoracic aorta in vitro were investigated using a rat platelet antiaggregatory bioassay and HPLC methods. The 2.5% beverages did not affect PGI2 synthesis; however, the 5% beverages significantly decreased PGI2 synthesis. The observed decreases were significantly abolished in presence of exogenous arachidonic acid suggesting a beverage-induced inhibition of precursor release. The ability of the beverages to inhibit PGI2 synthesis may partly contribute towards better understanding of the biochemical mechanisms underlying some of the beverages-induced actions in vivo.
Subject(s)
Aorta/metabolism , Coffee , Epoprostenol/biosynthesis , Tea , Animals , Drinking , Male , Rats , Rats, Inbred StrainsABSTRACT
The influence of sesame and cod liver oils (0.5 and 1 g/kg/day s.c. for 2 weeks) on arterial PGI2 synthesis in the rat was investigated using a rat platelet antiaggregatory bioassay and HPLC methods. Smaller doses did not affect PGI2 synthesis. However, sesame oil at a dose of 1 g/kg/day significantly stimulated PGI2 synthesis, whereas cod liver oil at the same dose significantly decreased the synthesis. Incubation of control tissues in presence of exogenous arachidonic acid (33 microM) significantly stimulated PGI2 synthesis, however, incubation of cod liver oil-treated tissues in presence of arachidonic acid resulted in PGI2 synthesis, similar to that observed in the nontreated controls. The changes observed in PGI2 synthesis in the tissues from oil-treated rats may have resulted from modulation in arachidonic acid release and/or direct effects on the enzymes involved in PGI2 synthesis. The oil-induced changes in PGI2 synthesis may partly contribute towards better understanding of the biochemical mechanisms that underly some of the in vivo actions of these oils.