AbstractInjection ofD‐myo‐inositol‐1,4,5‐trisphosphate (IP3) was found to induce a transient increase of intracellular Ca2+concentration in cancerous mammary cells (MMT060562) and in normal mammary cells treated with epidermal growth factor. Responses to injection of eitherD‐myo‐inositol‐1,4‐bisphosphate (IP2) orD‐myo‐inositol‐1,3,4,5‐tetrakisphosphate (IP4) were small or absent. Furthermore, normal mammary cells cultivated with low‐protein serum replacement alone or in the presence of differentiation‐inducing hormones (insulin + cortisol + prolactin) were less sensitive to IP3.Thapsigargin induced a transient increase of Ca2+due to the release of Ca2+from an intracellular pool. There was no difference in the peak heights of the thapsigargin‐induced Ca2+increase when mammary cells were cultivated in the presence or absence of epidermal growth factor or insulin + cortisol + prolactin. These findings suggest that the releasable intracellular Ca2+pool remained unchanged whereas sensitivity to IP3 increases during the proliferation stage.Mechanical stimulus of a mammary cell induces an increase of intracellular Ca2+in the stimulated cell. A certain stimulating factor is released from the mechanically stimulated cell into the extracellular space, and it induces an increase of Ca2+in surrounding cells.18In contrast, the IP3‐induced Ca2+increase in both cancerous and epidermal growth factor‐treated normal mammary cells did not spread to adjacent cells. Therefore, increase of Ca2+is not sufficient to account for the release of stimulating substances from mammary cells in the mechan