Agonists linked to the phosphoinositide signaling pathway evoke capacitative calcium entry in Xenopus oocytes. This entry pathway can also be activated by injection of inositol 2,4,5-trisphosphate, application of thapsigargin, or incubation in calcium-free medium. A variety of protocols revealed highly nonlinear behavior of the calcium entry in thapsigargin-treated oocytes suggestive of positive and negative feedback by calcium at the level of its own entry. These feedback mechanisms may account for the highly damped calcium oscillations we observed in thapsigargin-treated oocytes. Low level activation of protein kinase C potentiated calcium influx in thapsigargin-treated oocytes, apparently by blocking the inactivation of the calcium influx. Higher levels of protein kinase C activity inhibited capacitative calcium entry.