McCaa R E, Langford H G, Montalvo J M, Andy O J, Read V H, McCaa C S
Hypertension. 1981 May-Jun;3(3 Pt 2):I74-80. doi: 10.1161/01.hyp.3.3_pt_2.i74.
The aldosterone response to adrenocorticotropic hormone (ACTH) and angiotensin II (AII) was evaluated in patients with pituitary insufficiency before and after dietary sodium restriction (10 mEq Na+/day for 12 days). On normal sodium intake, plasma aldosterone concentration and plasma cortisol concentration failed to change from control levels in response to a single injection of ACTH or to a continuous 1-hour infusion of AII in patients with pituitary insufficiency. In response to dietary sodium restriction for 12 days, plasma renin activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 +/- 3.1 before and 12.3 +/- 3.7 ng/dl (ns, p greater than 0.05) after sodium deficiency. Although aldosterone secretion failed to increase during sodium deficiency, the patients came into balance at 10 mEq without a significant change in arterial blood pressure (BP). In sharp contrast to the lack of aldosterone response to ACTH before sodium deficiency, plasma aldosterone concentration increased markedly from 12.9 +/- 3.3 to 156 +/- 17.3 ng/dl (p less than 0.001) in response to ACTH after sodium deficiency. Although the adrenal glomerulosa cells were markedly sensitive to ACTH during sodium deficiency, they remained almost totally refractory to AII since aldosterone secretion failed to increase significantly in response to continuous infusion of a pressor dose of AII for 1 hour. Replacement therapy with ACTH gel for 3 months in patients with pituitary insufficiency failed to restore a normal aldosterone response to either ACTH or AII. These data demonstrate that some non-ACTH pituitary factor(s) is essential for a normal aldosterone response to ACTH, AII, and sodium deficiency.
在饮食限钠（10 毫当量钠/天，持续 12 天）前后，对垂体功能不全患者的醛固酮对促肾上腺皮质激素（ACTH）和血管紧张素 II（AII）的反应进行了评估。在正常钠摄入情况下，垂体功能不全患者单次注射 ACTH 或持续 1 小时输注 AII 后，血浆醛固酮浓度和血浆皮质醇浓度均未从对照水平发生变化。在饮食限钠 12 天后，垂体功能不全患者的血浆肾素活性（PRA）增加了五倍，而血浆醛固酮浓度未能显著增加，缺钠前平均为 11.0±3.1，缺钠后为 12.3±3.7 纳克/分升（无显著差异，p＞0.05）。尽管缺钠期间醛固酮分泌未能增加，但患者在 10 毫当量时达到平衡，动脉血压（BP）无显著变化。与缺钠前醛固酮对 ACTH 缺乏反应形成鲜明对比的是，缺钠后血浆醛固酮浓度因 ACTH 而从 12.9±3.3 显著增加至 156±17.3 纳克/分升（p＜0.001）。尽管缺钠期间肾上腺球状带细胞对 ACTH 明显敏感，但它们对 AII 几乎完全无反应，因为持续输注升压剂量的 AII 1 小时后醛固酮分泌未能显著增加。垂体功能不全患者用 ACTH 凝胶替代治疗 3 个月未能恢复醛固酮对 ACTH 或 AII 的正常反应。这些数据表明，某些非 ACTH 垂体因子对于醛固酮对 ACTH、AII 和缺钠的正常反应至关重要。
