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Modulation of Tissue Responsiveness to Angiotensin-II in Hyperprolactinemic Subjects^*

Division of Hypertension and Endocrinology, University Hospitals of Cleveland and Case Western Reserve University, and the Department of Epidemiology and Biostatistics, Case Western Reserve University Cleveland, Ohio 44106

Address all correspondence and requests for reprints to: B. M. Arafah, M.D., Department of Medicine, Division of Hypertension and Endocrinology, University Hospitals of Cleveland, 2074 Abington Road, Cleveland, Ohio 44106.

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.

^* This work was supported by a grant to the Clinical Research Center from the General Clinical Research Center and partially by a grant from the Northeast Ohio Affiliate of the American Heart Association (to B.M.A.), NIH Grant HL-22990 (to J.G.D.), and NIH Grant HL-39012 (to J.G.D.).

Received December 14, 1989.

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