Interactions of Prolactin and Adrenocorticotropin in the Regulation of Adrenocortical Secretions in Female Rats*

Abstract

Effects of PRL and ACTH alone and in combination upon adrenal function of hypophysectomized female rats were examined in vivo and in vitro. In vivo studies consisted of measuring hormone concentrations in peripheral plasma and in the venous effluent of the left adrenal gland. Secretion rates of corticosterone and its principal reduced metabolites [5α-dihydrocorticosterone (DHB) and 3β,5α-tetrahydrocorticosterone (THB)] were calculated. Adrenal 5α-reductase activity and production of corticosterone and total corticoids by adrenal homogenates and adrenal slices were studied in vitro. Removal of the pituitary elevated adrenal 5α-reductase activity. As a result, corticosterone was rapidly converted to DHB and THB. Administration of PRL to hypophysectomized rats resulted in decreased adrenal 5α-reductase activity and concomitantly increased the secretion of corticosterone in adrenal effluent by 79%. The peripheral plasma concentration of corticosterone was enhanced similarly. Secretion of corticosterone relative to that of its reduced metabolites was likewise enhanced by PRL in vivo and in vitro. ACTH markedly increased the secretion rates of corticosterone, DHB, and THB in adrenal effluent and enhanced the concentration of corticosterone in peripheral blood. ACTH also produced a significant decline in 5α-reductase activity which led to greater proportionate secretion of corticosterone relative to its reduced metabolites, DHB and THB. PRL given with ACTH potentiated the effect of ACTH on 5α-reductase by completely suppressing enzyme activity, which caused a concomitant rise in corticosterone secretion in vitro. As a consequence, proportionate output was enhanced 36% above that produced by ACTH alone. The results suggest that PRL plays a significant role in maintenance of corticosterone secretion, principally as a potent inhibitor of adrenal 5α-reductase when administered alone to hypophysectomized rats and in combination with ACTH. ACTH, on the other hand, seems to stimulate precursor availability as well as to inhibit 5α-reductase activity.