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Angiotensin II Promotes Prolactin Release from Normal Human Anterior Pituitary Cell Cultures in a Calcium-Dependent Manner^*

Departments of Internal Medicine and Physiological Chemistry, Ohio State University Columbus, Ohio 43210

Address requests for reprints to: William B. Malarkey, M.D., Ohio State University Medical Center, N-1106 Doan Hall, Columbus, Ohio 43210.

Renin and angiotensin II (All) have been demonstrated in the mammalian central nervous system, and All has been found to promote PRL release in the rat and monkey. We added All to monolayer cultures of human anterior pituitary cells and found significant PRL release by 30 min with concentrations of All as low as 10^–10 M. This All-induced PRL release was inhibited by the specific All antagonist saralasin. All-induced PRL release was a calcium-dependent process, since the calcium channel blockers verapamil and nifedipine as well as the calcium-calmodulin antagonist R2471 significantly inhibited All-induced PRL release. Prostaglandins E₂, A₂, and F₂ also inhibited All-induced PRL release. The significance of this latter observation is not clear, however, as indomethacin, an inhibitor of the cyclo-oxygenase prostaglandin metabolic pathway, had no effect on All-induced PRL release. In light of recent immunohistochemical evidence of the presence of renin, angio-tensinogen, and converting enzyme in humal lactotrophs, our data support the concept that AH may be an important autocrine regulator of PRL secretion.

^* This work was supported in part by NIH Grants R01-CA33213 and CA-16058, General Clinical Research Center Grunt RR-34, and the Mary Gertmenian Cancer Research Fund.

Received August 25, 1986.

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