Central control of intestinal motility by prostaglandins: a mediator of the actions of several peptides in rats and dogs.

The effect of intracerebroventricular and intravenous administrations of prostaglandin E2 on gastrointestinal motility were investigated in conscious rats and dogs using electrodes and strain gauges, respectively. Injections were performed during the fed state and the motor changes were compared with those after intracerebroventricular administration of calcitonin, neurotensin, and (D-Ala2, Met5) enkephalinamide. Intracerebroventricular administration of prostaglandin E2 (0.5 micrograms) to fed rats restored the migrating myoelectric complex for 67 +/- 16 min. A migrating myoelectric complex-restoring effect was also observed after intracerebroventricular administration of calcitonin (0.02 U) and neurotensin (80 ng). This effect was blocked by previous intracerebroventricular administration of indomethacin (0.25 mg). Administered centrally to dogs but not intravenously at a 10-fold greater dose, prostaglandin E2 (0.1 microgram/kg) reduced (52.8%) the duration of the jejunal postprandial motor state similarly to that observed after intracerebroventricular administration of calcitonin (0.1 U/kg), neurotensin (0.1 microgram/kg), and (D-Ala2, Met5) enkephalinamide (0.1 microgram/kg). These effects of calcitonin and neurotensin were abolished 4 h after an intramuscular injection of indomethacin (2 mg/kg), whereas those of (D-Ala2, Met5) enkephalinamide persisted. These results suggest that (a) prostaglandins act centrally to control the pattern of intestinal motility in both rats and dogs and (b) calcitonin and neurotensin when injected intracerebroventricularly affect the intestinal motor profile probably by stimulating prostaglandin release within the brain.