Prostaglandin E2 and prostaglandin F2 regulation of triglyceride levels in uterine smooth muscle from restricted-diet estrous and diestrous rats.

Triglyceride concentrations in uterine strips isolated from estrous and diestrous normal-fed or restricted-diet (50% food intake for 15 days) rats, were measured. Determinations were made immediately following killing (0 min, or postisolation) as well as after a period in glucose-free medium, (60 min or post-incubation) with or without additions. The postisolation levels of triglycerides (0 min) in the uterus from normal-fed estrous animals were lower than in diestrus but in each group did not differ in comparison with postincubation values (60 min), either without additions or in the presence of indomethacin (10-6M). Initial (0 min) tissue triglycerides of estrous and diestrous partially-starved rats were significantly higher than in their respective fed controls and exhibited different modifications depending on the stage of the sex cycle. In estrus, levels remained unaltered at the end of an incubating period without additions and declined in the presence of indomethacin. This influence of indomethacin was not modified by added PGF2 (10(-9)M) but was effectively abolished by PGE2 (10(-9)M). On the contrary, in diestrus, initial triglyceride levels diminished spontaneously following 60 min without additions, this being antagonized by indomethacin or propranolol (10(-6)M). Furthermore, exogenous PGE2 failed to alter the effect of indomethacin whereas PGF2 evoked its abolition. Propranolol, which effectively blocked the spontaneous decrement of triglycerides as did indomethacin, prevented also the influence of PGF2 on the action of indomethacin. The foregoing results are compatible with the notion that the regulation of triglycerides in rat uteri suspended in the absence of exogenous substrate, is affected differently by prostaglandin E2 and F2 alpha depending on the state of the sex cycle. They also suggest that the phenomenon may involve the activation of the beta adrenoreceptors.