Angiotensin II and dopamine modulate both cAMP and inositol phosphate productions in anterior pituitary cells. Involvement in prolactin secretion.
نویسندگان
چکیده
Despite their opposite effects on prolactin secretion, both dopamine and angiotensin II inhibit adenylate cyclase activity in homogenates of anterior pituitary cells in primary culture. Dopamine and angiotensin II inhibition of adenylate cyclase was not additive, suggesting that both neurohormones inhibit the adenylate cyclase of the lactotroph cells. Pretreatment with Bordetella pertussis toxin (islet activator protein) completely suppressed the dopamine-induced inhibition of both adenylate cyclase and prolactin secretion. The islet activator protein also reversed the angiotensin II-induced inhibition of the adenylate cyclase activity. In contrast, angiotensin II stimulation of prolactin release was not affected by the toxin. Angiotensin II also induced a dose-dependent stimulation of inositol phosphates (250%) with an EC50 of 0.1 nM, close to that observed for prolactin secretion. Islet activator protein pretreatment did not block the stimulation of inositol phosphate production. Dopamine inhibited the angiotensin II-stimulated prolactin release and the production of inositol phosphates induced by angiotensin II. It is concluded that angiotensin II and dopamine receptors of lactotroph cells are able to modulate both cAMP and inositol phosphate production. The dopamine receptor of lactotrophs appears to be the first example of a receptor which is negatively coupled to the production of inositol phosphates.
منابع مشابه
Desensitization of angiotensin II: effect on [Ca]i, inositol triphosphate, and prolactin in pituitary cells
González Iglesias, Arturo, Cecilia Suárez, Claudia Feierstein, Graciela Dı́az-Torga, and Damasia BecuVillalobos. Desensitization of angiotensin II: effect on [Ca]i, inositol triphosphate, and prolactin in pituitary cells. Am J Physiol Endocrinol Metab 280: E462–E470, 2001.—Activation of pituitary angiotensin (ANG II) type 1 receptors (AT1) mobilizes intracellular Ca , resulting in increased prol...
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ورودعنوان ژورنال:
- The Journal of biological chemistry
دوره 261 9 شماره
صفحات -
تاریخ انتشار 1986