Judd A M, Koike K, Schettini G, Login I S, Hewlett E L, Yasumoto T, MacLeod R M
Endocrinology. 1985 Sep;117(3):1215-21. doi: 10.1210/endo-117-3-1215.
The rat pituitary tumor 7315a secretes PRL and ACTH. Although dopamine has no effect on unstimulated PRL release from this tumor, dopamine decreases the adenylate cyclase activity in tumor cell homogenates in a manner similar to that in normal pituitary tissue. However, it was observed that under basal conditions, 7315a tumor cells have an abnormal calcium metabolism because 1) basal PRL release from tumor cells is not modified by the calcium channel blocker D-600 and is only moderately decreased by low calcium, treatments that markedly decrease normal pituitary PRL release; 2) D-600 had no effect on basal 7315a tumor calcium uptake, but blocked the increase in calcium uptake due to the calcium channel activator maitotoxin; 3) increasing the medium Ca+2 concentration above 5 mM increases 7315a PRL release, whereas this treatment decreases PRL release from normal pituitary cells. Maitotoxin and the calcium ionophore A23187 increased 7315a tumor cell PRL release in a manner similar to that in normal pituitary cells. Because dopamine blocks PRL release induced by maitotoxin, A23187, or elevated medium calcium concentration in 7315a tumor cells, the refractoriness of basal 7315a tumor cell PRL release to dopamine may be due to the abnormal calcium balance of the tumor cells under basal conditions.
