Prostaglandins

Since the literature on PGs (prostaglandins) is increasing so rapidly, this literature review covers only the following PG-related topics: 1) PG biosynthesis; 2) PG metabolism; 3) analysis of PGs; 4) PG receptors; 5) PGs and cyclic nucleotides; and 6) the effect of PGs on platelet function. PG biosynthesis has been monitored by labeled precursor acids and chromatographic identification, gas-liquid chromatography, radioimmunoassay and multiple ion analysis, and measurement of urinary metabolites. These methods have shown that many mammalian tissues produce PGs. Various conditions and agents have been found to alter the rate of PG synthesis; aspirin is 1 agent which inhibits PG biosynthesis. The metabolic pathways of PGs are diagrammed chemically. The highly sensitive methods for performing quantitative analysis of PGs which have been developed in recent years are explained. These include gas chromatography with electron capture detectors, gas chromatography/mass spectrometry, and radio-immunoassay. PGs are known to react with adenyl cyclase in many different tissues. This may explain their wide variety of pharmacological effects. Platelet aggregation is stimulated in its 2nd stage by PGE2 and inhibited by PGE1.