MODULATION OF TISSUE RESPONSIVENESS TO ANGIOTENSIN-II IN HYPERPROLACTINEMIC SUBJECTS

The present studies were designed to test the hypothesis that hyperprolactinemia modulates target tissue responsiveness to angiotensin-II (AII). Adrenal and pressor responses to All infusions were determined in six patients with PRL-secreting pituitary microadenomas and in five normal controls during defined electrolyte balance. Hyperprolactinemic and normal subjects had similar mean blood pressures while on a regular Na intake (82.5 ± 0.5 vs. 81.2 ± 0.3 mm Hg). However, after 4 days of Na loading (200 meq/day), the mean blood pressure in hyperprolactinemic subjects was higher than that in normal (86.6 ± 1 vs. 83.4 ± 0.8 mm Hg; P < 0.05). In addition, enhancement of the mean blood pressure response to three doses of All was noted in hyperprolactinemic subjects (P < 0.05) compared to that in normal subjects. After 4 days of Na restriction (10 meq/day), the mean blood pressure in hyperprolactinemic subjects was similar to that in normal subjects (79.7 ± 0.6 vs. 78.9 ± 1 mm Hg). However, despite adequate Na restriction, the pressor response to AII continued to be enhanced (P < 0.05) in hyperprolactinemic subjects. There were no differences in plasma or urinary electrolytes or in PRA between hyperprolactinemic and normal subjects. Hyperprolactinemic subjects had higher basal (P < 0.01), AII-stimulated (P < 0.05), and ACTH-stimulated (P < 0.02) aldo-sterone levels during Na loading, but not during Na restriction. The differences disappeared after the correction of the hyper-prolactinemia. The data demonstrate significant alterations in adrenal and pressor responsiveness in hyperprolactinemic subjects and suggest a modulating role for PRL on vascular reactivity and steroid biosynthesis. The precise mechanism has not been determined, but may be secondary to PRL-induced up-regulation of adrenal and vascular All receptors. © 1990 by The Endocrine Society.