Intestinal myoelectric activity was measured in four conscious dogs with implanted monopolar electrodes after administration of prostaglandins (PG) and indomethacin (Indo), a potent inhibitor of PG biosynthesis. PGE2 and PGI2 given intravenously caused a dose-dependent decrease in the frequency of the migrating myoelectric complex (MMC) in fasted dogs and in postprandial spike activity in fed animals. In contrast, PGF2 alpha interrupted the MMC and caused a fedlike pattern in fasted dogs and did not affect the postprandial spike activity. Similar effects were observed after intra-arterial infusion of PGs. PGE2 and PGI2 infused into the superior mesenteric artery caused a dose-dependent inhibition of the fasted and postprandial pattern of myoelectric activity of the small bowel, whereas PGF2 alpha blocked the MMC and increased spike activity. Indo injected in a single intravenous dose caused a significant reduction in the MMC interval, and Indo infused intravenously in a constant dose induced fedlike motility pattern in fasted dogs but had little effect on the postprandial activity in these animals. This study demonstrates that exogenous PGs of E and I series administered intravenously or intra-arterially inhibit intestinal motility, whereas PGF2 alpha has opposite effects. The finding that Indo increases intestinal motility indicates that endogenous PGs are important in the physiological control of intestinal motility.