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Is prolactin playing a role in the regulation of catecholamine synthesis and release from male rat adrenal medulla?

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Abstract

Previous evidence allows one to suspect that prolactin (PRL) may be a physiological regulator of catecholamine (CA) synthesis and release in the adrenal gland of rodents. To explore this possibility, we studied the in vivo and in vitro metabolism and release of noradrenaline (NA) and adrenaline (A) in the adrenal gland of male rats. The study was carried out with animals exhibiting a moderate increase in plasma PRL levels induced by grafting of additional pituitaries or a severe hyperprolactinemia produced by diethylstilbestrol (DES)-induced pituitary hyperplasia. The latter animals exhibited a significant increase in adrenal weight, associated with decrease in tyrosine hydroxylase (TH) activity and in NA content. Moreover, the adrenal activity of phenylethanolamine-N-methyl transferease (PNMT) was decreased in DES-treated animals. Pituitary-grafted rats also displayed an increased adrenal weight, together with decreases in the activities of PNMT, catechol-O-methyl tansferase and monoamine oxidase. These in vivo observations were followed by in vitro studies, which showed a decrease in the basal release of both CAs from incubated adrenals of DES-treated rats, with no changes in pituitary-grafted rats. In addition, exposure to PRL of the incubated adrenals of animals exhibiting normal PRL levels produced decreases in A release and storage and in TH activity. These observations allow us to conclude that: i) PRL appears to exert an inhibitory influence on the catecholaminergic activity in the adrenal gland; and ii) its effect seems to be exerted by a direct action on this gland.

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A preliminary report of this work has been presented and published in abstract form at the “III Congreso Hispano-Luso de Bioquímica, Santiago de Compostela, 1988”.

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Hernández, M.L., de Miguel, R., Ramos, J.A. et al. Is prolactin playing a role in the regulation of catecholamine synthesis and release from male rat adrenal medulla?. J Endocrinol Invest 14, 201–208 (1991). https://doi.org/10.1007/BF03346789

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