Beta-Adrenergic Stimulation of Anterior Pituitary Cyclic Amp is Enhanced by Tumor Promoters

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Abstract
Beta-adrenergic stimulation of cellular cyclic AMP accumulation was characterized in normal anterior pituitary cells in vitro. In the presence of isobutylmethylxanthine, the order of potency of cate-cholamine agonists, as well as the antagonism by propranolol and not phentolamine, aided in classifying the receptor as beta-adrenergic. Furthermore, this agonist effect was rapidly desensitized. Tumor promoters, which directly activate protein kinase C, enhanced the cyclic AMP levels achieved with beta-adrenergic agonists (1.5-fold average at 10 min). This acute effect occurred over 10 - 1000 nM phorbol dibutyrate or phorbol myristate acetate. Finally, 3H-phorbol dibutyrate binding to unstimulated anterior pituitary cells was predominately associated with the cytosol (79%) versus membrane (21%) fractions. Thus, an acute role for protein kinase C in promoting beta-adrenergic receptor activation of adenylate cyclase activity is suggested for anterior pituitary cells.

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