Inositol phosphates have an important role in Ca²⁺ mobilization and especially inositol 1, 4, 5-trisphosphate (IP₃) is now believed to release Ca²⁺ from the endoplasmic reticulum (ER) . On the other hand, the mechanism of activation of Ca²⁺ entry is unknown. Non-excitable cells have only receptoroperated Ca²⁺ channels, lacking voltage-operated Ca²⁺ channels, and are a useful system for studying signal transduction. In this review, some mechanisms for the regulation of Ca²⁺ entry in non-excitable cells are discussed and a new hypothesis originally proposed by Putney (1986), the capacitative Ca²⁺ entry model, is focussed. In this model, Ca²⁺ influx across the plasma membrane is increased when the IP3-sensitive Ca²⁺ pools is emptied. Capacitative Ca²⁺ entry is now confirmed in rat parotid acinar cells by studies on the refilling process for intracellular Ca²⁺ pools and by using the microsomal Ca²⁺ATPase inhibitor thapsigargin, which does not increase cellular IP₃. Finally, capacitative Ca²⁺ entry is expected to exist in a variety of cell types including excitable cells.