Mizuno K, Gotoh M, Haruyama K, Yamazaki M, Shigetomi S, Matsui J, Fukuchi S
Nihon Naibunpi Gakkai Zasshi. 1981 Aug 20;57(8):1109-17. doi: 10.1507/endocrine1927.57.8_1109.
The response of plasma aldosterone to exogenous angiotensin II was evaluated in five normal volunteers on three occasions, once without endogenous ACTH or angiotensin II suppression (control), once with ACTH suppression (dexamethasone) and once with ACTH and angiotensin II suppression (dexamethasone and captopril). Plasma aldosterone concentration (PAC) fell from a control of 6.8 +/- 1.6 (mean +/- SEM) to 4.4 +/- 0.4 ng/dl with dexamethasone (p less than 0.05) and to 1.8 +/- 0.2 ng/dl with dexamethasone and captopril (p less than 0.001). PAC increased dose-dependently upon infusion rates of angiotensin II (0.2, 0.4, 0.8, 1.0, 1.2, 2.5 and 5.0 ng/kg/min) on each occasion, but aldosterone responsiveness to infused angiotensin II (change and percentage from base line levels) was not altered by the suppression of endogenous ACTH secretion with dexamethasone with each incremental infusion of the octapeptide. However, change in PAC caused by angiotensin II in the suppression of ACTH and angiotensin II was greater than that in the control at an infusion rate of 0.2 ng/kg/min (p less than 0.05), 1.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01), and it was also greater than that in the suppression of ACTH at an infusion rate of 0.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01). These results demonstrate that in normal men, base line aldosterone levels are controlled not only by the renin-angiotensin system, but also, in part, by ACTH. The aldosterone response to angiotensin II, however, does not depend upon endogenous ACTH secretion, an action of angiotensin II on the pituitary to release ACTH. Simultaneous administration of dexamethasone and captopril may be a useful tool to assess the sensitivity of aldosterone production in the adrenal glomerulosa with exogenous angiotensin II since endogenous ACTH and angiotensin II can be suppressed by these medications.
在五名正常志愿者身上分三次评估了血浆醛固酮对外源性血管紧张素II的反应,一次不抑制内源性促肾上腺皮质激素(ACTH)或血管紧张素II(对照),一次抑制ACTH(地塞米松),一次同时抑制ACTH和血管紧张素II(地塞米松和卡托普利)。血浆醛固酮浓度(PAC)从对照时的6.8±1.6(均值±标准误)降至使用地塞米松时的4.4±0.4 ng/dl(p<0.05),降至使用地塞米松和卡托普利时的1.8±0.2 ng/dl(p<0.001)。每次给予血管紧张素II(0.2、0.4、0.8、1.0、1.2、2.5和5.0 ng/kg/min)时,PAC均呈剂量依赖性增加,但在每次递增输注八肽时,使用地塞米松抑制内源性ACTH分泌并未改变醛固酮对输注血管紧张素II的反应性(相对于基线水平的变化和百分比)。然而,在抑制ACTH和血管紧张素II时,血管紧张素II引起的PAC变化在输注速率为0.2 ng/kg/min(p<0.05)、1.2 ng/kg/min(p<0.05)和2.5 ng/kg/min(p<0.01)时大于对照,并且在输注速率为0.2 ng/kg/min(p<0.05)和2.5 ng/kg/min(p<0.01)时也大于抑制ACTH时。这些结果表明,在正常男性中,基线醛固酮水平不仅受肾素-血管紧张素系统控制,还部分受ACTH控制。然而,醛固酮对血管紧张素II的反应并不依赖于内源性ACTH分泌,即血管紧张素II对垂体释放ACTH的作用。同时给予地塞米松和卡托普利可能是一种有用的工具,可用于评估外源性血管紧张素II作用下肾上腺球状带醛固酮生成的敏感性,因为这些药物可抑制内源性ACTH和血管紧张素II。