Delayed gastric emptying is a common problem in preterm infants. The factors underlying this gastroparesis remain unsettled but may involve immaturity of smooth muscle contraction. The present study was designed to test this hypothesis. Muscle strips from the gastric fundus of fetal and adult guinea pigs were studiedin vitrofor their contractile response to receptor activation (acetylcholine and bethanechol) and membrane depolarization (potassium chloride). The dose-response curves were analyzed for differences in active force development (kg/cm2). The role of extracellular calcium (Ca2+) in the contractile responses was determined by contracting the tissues in a zero-Ca2+physiologic saline solution and in the presence of nifedipine, a voltage-dependent Ca2+channel blocker. The results demonstrate the following:1) tissues from adult animals developed significantly more active force when tested with acetylcholine, bethanechol, and potassium chloride;2) tissues from the fetal animals were relatively unresponsive to contraction with potassium chloride compared with the adult; and3) both nifedipine and incubation in a zero-Ca2+physiologic saline solution had a significantly greater inhibitory effect on the contractions of adult than fetal muscle strips. Our data indicate that smooth muscle in the gastric fundus develops increasing force with maturation. The increased contractility in the adult fundus appears to be due to an increased involvement of extracellular calcium influx, in part through voltage-dependent Ca2+channels.