In VitroStudies on Prolactin Release and Adenylate Cyclase Activity in Human Prolactin-Secreting Pituitary Adenomas. Different Sensitivity of Macro- and Microadenomas to Dopamine and Vasoactive Intestinal Polypeptide*

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Abstract
A number of human PRL-secreting pituitary adenomas were tested for their in vitro responsiveness to dopamine (DA) and vasoactive intestinal polypeptide (VIP). PRL release from tumor fragments and adenylate cyclase (AC) activity in membrane fractions were evaluated. Both the hormone release and the enzyme activity were found to be inhibited by DA and stimulated by VIP. Significant differences between microadenomas (diameter less than 10 mm) and macroadenomas have been demonstrated: 1) the basal secretory activity (calculated per milligram of tissue protein) was higher in macro- than in microprolactinomas; 2) PRL release and AC activity were inhibited by a given concentration of DA to a higher extent in macro- than in microadenomas; 3) the dose-effect curves of DA both on PRL release and AC activity showed that the potency, and, in some cases, also the efficacy of the catecholamine was greater in macro- than in microadenomas; 4) PRL release and AC activity were stimulated by a given concentration of VIP to a higher extent in micro- than in macroadenomas; 5) the doseeffect curves showed that VIP efficacy was higher in micro- thanin macroadenomas, whereas no significant difference in potency could be revealed. In macroadenomas, NaF and (Bu)2cAMP stimulated AC activity and PRL release, respectively, to a much higher extent than VIP, suggesting that the intracellular secretory processes were not already maximally stimulated. Therefore, a difference in number of receptors for the peptide in macro- and microadenomas has been hypothesized. Taken together, these findings show that macro- and microprolactinomas differ by more than just size. In addition, the close parallelism between PRL release and AC activity in response to both agents strongly supports the hypothesis of an involvement of cAMP in the intracellular mechanisms by which DA and VIP regulate PRL release in adenomatous mammotrophs.

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