Glorioso N, Dessì-Fulgheri P, Alagna S, Rubattu S, Soro A, Madeddu P, Bandiera F, Masala A, Rovasio P P, Rappelli A
Clin Exp Hypertens A. 1987;9(2-3):665-70. doi: 10.3109/10641968709164239.
To investigate the role of Angiotensin II in the release of ACTH, the response of adrenocorticotrophic hormone to hypoglycaemia was studied before and during treatment with an angiotensin converting enzyme inhibitor, enalapril, in 15 male patients with essential hypertension. Plasma levels of ACTH were measured before and 60, 90 and 120 min after an i.v. bolus of normal saline, as placebo, and, 3 days later, after an i.v. bolus of regular insulin (0.15 U/Kg b.w.). Enalapril treatment was then started and both placebo and hypoglycaemic tests were repeated 15 days thereafter. No changes in ACTH plasma levels were observed after acute normal saline either before or during enalapril treatment. On the contrary, hypoglycaemia induced a sharp increase of ACTH before enalapril (from 19.5 +/- 4.1 to 74.4 +/- 13.0 pg/ml, p less than 0.01 60 min after insulin) but not during ACE inhibition (from 26.1 +/- 6.2 to 34.6 +/- 5.9 pg/ml, NS, at min 60 of the study). The present data confirm our previous observation on the reduction of the hypoglycaemic-induced ACTH release during ACE inhibition with captopril and support the hypothesis that circulating Ang II may exert a facilitating role on adrenocorticotrophic hormone release.
为研究血管紧张素II在促肾上腺皮质激素（ACTH）释放中的作用，我们对15名原发性高血压男性患者在使用血管紧张素转换酶抑制剂依那普利治疗前及治疗期间，研究了促肾上腺皮质激素对低血糖的反应。在静脉推注生理盐水作为安慰剂前以及推注后60、90和120分钟测量血浆ACTH水平，3天后，静脉推注正规胰岛素（0.15 U/Kg体重）后再次测量。然后开始依那普利治疗，15天后重复安慰剂和低血糖试验。在依那普利治疗前及治疗期间，急性输注生理盐水后未观察到血浆ACTH水平变化。相反，低血糖在依那普利治疗前可引起ACTH急剧升高（胰岛素注射后60分钟，从19.5±4.1升至74.4±13.0 pg/ml，p<0.01），但在血管紧张素转换酶（ACE）抑制期间未出现这种情况（研究60分钟时，从26.1±6.2升至34.6±5.9 pg/ml，无统计学意义）。目前的数据证实了我们之前关于卡托普利抑制ACE期间低血糖诱导的ACTH释放减少的观察结果，并支持循环中的血管紧张素II可能对促肾上腺皮质激素释放起促进作用的假说。
