Isolated strips of mid-pregnant and postpartum rat myometrium were rendered functionally Ca2-free by exposure to a Ca2-free modified Krebs-bicarbonate solution containing 1 mM ECTA. The muscle strips were then exposed to 2.25 mM Ca2for periods of 15 to 600 seconds for the mid-pregnant tissues and one 120-second period for the postpartum tissues. At the end of each exposure. Ca2was removed and simultaneously each muscle was depolarized with 125 mM K2SO2. Isometric tension changes in the muscles were measured with and without 0.5 per cent halothane. In the mid-pregnant muscles, halothane diminished the initial tension development in response to Ca2by approximately 50 per cent, regardless of the duration of Ca2exposure. The contractile response of these muscles to depolarization with K2SO4was reduced 10 per cent by 0.5 per cent halothane; this was probably due to reduction in transmembrane influx of Ca2. In the postpartum muscles, the initial tension development in response to Ca2was threefold greater than in mid-preguaut muscles and was reduced 25 per cent by halothane. These tissues failed to develop any tension in response to K2SO4. The most likely explanation for the effect of halothane is that it reduces the transmembrane influx of Ca2in both types of tissues, but that the postpartum sarcoplasmic reticulum presents less competition for intracellular Ca2than pregnant sarcoplasmic reticulum.