Lack of prolactin involvement in corticosteroid secretion.
In mammals prolactin can modify adrenal steroidogenesis. Its trophic effect on adrenal cells where prolactin receptors have been identified suggest a direct impact upon corticosteroid biosynthesis. In man, this role of prolactin remains controversial. The purpose of our study was to investigate the effects of chronic hyperprolactinemia on basal and stimulated corticosteroid hormone secretion. Seven women with untreated chronic hyperprolactinemia (HPRL) were included in the study. In each of them, a beta 1-24 ACTH test was performed on a normal and low Na+ diet for 4 days. Basal and ACTH-stimulated cortisol, aldosterone, deoxycorticosterone and 17 hydroxyprogesterone secretion were not significantly different in HPRL and NPRL women. These results do not support evidence for any significant role of prolactin upon corticosteroid biosynthesis in man. They also suggest that prolactin is not the pituitary factor which modulates ACTH or low Na+ diet stimulated corticosteroid secretion.
D019326:17-alpha-Hydroxyprogesterone; D000305:Adrenal Cortex Hormones / Q000378:metabolism*; D000311:Adrenal Glands / Q000378:metabolism; D000328:Adult; D000450:Aldosterone / Q000097:blood; D003366:Cosyntropin; D003900:Desoxycorticosterone / Q000097:blood; D004039:Diet, Sodium-Restricted; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006908:Hydroxyprogesterones / Q000097:blood; D006966:Hyperprolactinemia / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism*
D000305:Adrenal Cortex Hormones; D006908:Hydroxyprogesterones; D003366:Cosyntropin; D003900:Desoxycorticosterone; D000450:Aldosterone; D019326:17-alpha-Hydroxyprogesterone; D011388:Prolactin; D006854:Hydrocortisone