Denolle T, Rohmer V, Saint-Adnré J P, Guyene T T, Galland F, Bigorgne J C, Schambelan M, Corvol P
Hypertension Clinic, Hôpital Broussais, Paris, France.
J Clin Endocrinol Metab. 1990 Jan;70(1):288-92. doi: 10.1210/jcem-70-1-288.
We recently reported that renin, angiotensinogen, and angiotensin-converting enzyme were present in normal human pituitary lactotroph cells and PRL-secreting adenomas. Angiotensin-II and -III have also been shown to modulate PRL release in vitro. The present study was designed to determine whether angiotensin modulates PRL secretion in vivo. In 36 hypertensive patients with widely varying renin levels, active renin and basal PRL levels did not correlate. In 10 normal volunteers, both a sustained infusion of angiotensin-II and a graded infusion of angiotensin-III induced a 2- to 3-fold increase in aldosterone levels, but had no effect on PRL secretion. Administration of the angiotensin-converting enzyme inhibitor captopril had no effect on PRL circadian rhythm in 10 normal subjects or on PRL concentrations in 11 patients with PRL-secreting adenomas. Cross-over administration of placebo and captopril did not affect the peak PRL level measured after TRH treatment in 10 hypertensive men (placebo, 43.1 +/- 5.4; captopril, 40.0 +/- 6.2 micrograms/L; P = NS) or the rise in PRL induced by doperidone in 6 normal women (placebo, 129.5 +/- 16.2; captopril, 150.0 +/- 35.7 micrograms/L; P = NS). Further, administration of enalapril for 30 days to 6 hypertensive patients did not alter basal PRL concentrations or the peak concentrations induced by TRH. These data indicate that in humans the circulating renin-angiotensin system does not interact with diurnal PRL release or with the response to TRH or domperidone.
我们最近报道，正常人类垂体催乳素细胞和分泌催乳素的腺瘤中存在肾素、血管紧张素原和血管紧张素转换酶。血管紧张素-II和 -III在体外也已显示可调节催乳素释放。本研究旨在确定血管紧张素在体内是否调节催乳素分泌。在36名肾素水平差异很大的高血压患者中，活性肾素和基础催乳素水平不相关。在10名正常志愿者中，持续输注血管紧张素-II和分级输注血管紧张素-III均使醛固酮水平增加2至3倍，但对催乳素分泌无影响。给予血管紧张素转换酶抑制剂卡托普利对10名正常受试者的催乳素昼夜节律或11名分泌催乳素腺瘤患者的催乳素浓度无影响。在10名高血压男性中，安慰剂和卡托普利交叉给药不影响促甲状腺激素释放激素（TRH）治疗后测得的催乳素峰值水平（安慰剂，43.1±5.4；卡托普利，40.0±6.2微克/升；P =无显著性差异），在6名正常女性中，不影响多潘立酮诱导的催乳素升高（安慰剂，129.5±16.2；卡托普利，150.0±35.7微克/升；P =无显著性差异）。此外，对6名高血压患者给予依那普利30天，未改变基础催乳素浓度或TRH诱导的峰值浓度。这些数据表明，在人类中，循环肾素-血管紧张素系统不与催乳素的昼夜释放或对TRH或多潘立酮的反应相互作用。
