Olgaard K, Madsen S, Hammer M
Acta Med Scand. 1977;202(3):213-9. doi: 10.1111/j.0954-6820.1977.tb16814.x.
In the present study 8 anephric and 4 non-nephrectomized patients were stimulated with angiotensin II (A-II). In 5 of the anephric patients, an increased plasma aldosterone concentration (PAC) in response to ACTH stimulation had previously been demonstrated. After A-II stimulation, all 8 anephric patients responded with a significant rise in PAC although the increase was less pronounced than in 4 non-nephrectomized patients. In both groups of patients the increase in PAC was correlated to the increase in diastolic and systolic BP and to the A-II dose. Furthermore, in the non-nephrectomized patients, the plasma renin activity showed a significant decline, which was inversely correlated to the increase in PAC. When all 12 patients, regardless of the difference in remaining renin-angiotensin system, were considered as one population, the variable basal levels of PAC correlated significantly to the increase in PAC during A-II and ACTH stimulation. It is concluded that the adrenals of anephric man respond to A-II with an increase in PAC and that the reason for a lower response appears to be the lack of the renin-angiotensin system.
在本研究中，对8例无肾患者和4例未行肾切除术的患者用血管紧张素II（A-II）进行刺激。在5例无肾患者中，先前已证明其血浆醛固酮浓度（PAC）对促肾上腺皮质激素（ACTH）刺激有升高反应。A-II刺激后，所有8例无肾患者的PAC均显著升高，尽管升高幅度不如4例未行肾切除术的患者明显。两组患者的PAC升高均与舒张压和收缩压的升高以及A-II剂量相关。此外，在未行肾切除术的患者中，血浆肾素活性显著下降，这与PAC的升高呈负相关。当将所有12例患者，无论其剩余肾素-血管紧张素系统的差异如何，视为一个总体时，PAC的基础水平变化与A-II和ACTH刺激期间PAC的升高显著相关。结论是，无肾者的肾上腺对A-II有反应，导致PAC升高，反应较低的原因似乎是缺乏肾素-血管紧张素系统。
