Arafah B M, Gordon N H, Salazar R, Douglas J G
Division of Hypertension and Endocrinology, University Hospitals of Cleveland, Ohio 44106.
J Clin Endocrinol Metab. 1990 Jul;71(1):60-6. doi: 10.1210/jcem-71-1-60.
The present studies were designed to test the hypothesis that hyperprolactinemia modulates target tissue responsiveness to angiotensin-II (AII). Adrenal and pressor responses to AII 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 less than 0.05). In addition, enhancement of the mean blood pressure response to three doses of AII was noted in hyperprolactinemic subjects (P less than 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 less than 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 less than 0.01), AII-stimulated (P less than 0.05), and ACTH-stimulated (P less than 0.02) aldosterone levels during Na loading, but not during Na restriction. The differences disappeared after the correction of the hyperprolactinemia. 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 AII receptors.
本研究旨在验证高催乳素血症调节靶组织对血管紧张素II（AII）反应性的假说。在明确的电解质平衡状态下，测定了6例分泌催乳素的垂体微腺瘤患者和5例正常对照者对AII输注的肾上腺及升压反应。高催乳素血症患者和正常受试者在常规钠摄入量时平均血压相似（82.5±0.5对81.2±0.3mmHg）。然而，在钠负荷4天（200meq/天）后，高催乳素血症患者的平均血压高于正常受试者（86.6±1对83.4±0.8mmHg；P<0.05）。此外，与正常受试者相比，高催乳素血症患者对三剂AII的平均血压反应增强（P<0.05）。在钠限制4天（10meq/天）后，高催乳素血症患者的平均血压与正常受试者相似（79.7±0.6对78.9±1mmHg）。然而，尽管钠限制充分，但高催乳素血症患者对AII的升压反应仍持续增强（P<0.05）。高催乳素血症患者与正常受试者之间的血浆或尿电解质以及肾素活性无差异。高催乳素血症患者在钠负荷期间基础醛固酮水平较高（P<0.01）、AII刺激后醛固酮水平较高（P<0.05）、促肾上腺皮质激素刺激后醛固酮水平较高（P<0.02），但在钠限制期间无此情况。高催乳素血症纠正后差异消失。数据表明高催乳素血症患者的肾上腺及升压反应性有显著改变，并提示催乳素对血管反应性和类固醇生物合成具有调节作用。确切机制尚未确定，但可能继发于催乳素诱导的肾上腺和血管AII受体上调。
