Klumpp F, Klaus D, Lemke R, Zehner J, Zöfel P
Klin Wochenschr. 1975 Mar 1;53(5):221-9. doi: 10.1007/BF01468811.
Plasma aldosterone, plasma renin activity, sodium and potassium in the plasma and the urine were determinated under acute stimulation with saline-depletion (furosemide) and under acute suppression with saline infusion in 40 patients with primary hypertension stage I, 19 patients with primary hypertension stages II and III, and 11 patients with renal hypertension (chronic glomerulonephritis and chronic pyelonephritis). The majority of the patients with primary hypertension stage I showed a good stimulation of the plasma aldosterone and the plasma renin activity under acute salt depletion. Three out of the 40 patients with primary hypertension stage I, and 13 of the 19 patients with primary hypertension stages II and III did not show any stimulation of the renin secretion ("low renin hypertension"). In all these patients the plasma aldosterone stimulation remained intact. With infusion of saline all the groups showed suppression of the plasma aldosterone and the plasma renin activity. A good stimulation of the plasma renin activity, demonstrates that in our experiments the renin-angiotensin system cannot be responsible for the increase in aldosterone secretion under salt depletion. Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. In all patients with primary hypertension we did not find an inadequate reaction of the aldosterone secretion under saline infusion. The patients with renal hypertension showed a minimal stimulation and suppression of the plasma renin activity. The plasma aldosterone secretion increased only slightly under sodium depletion and the decrease under saline infusion was statistically not significant. Thus we conclude that these patients show an inadequate reaction of the plasma aldosterone and renin secretion under salt infusion and depletion.
对40例Ⅰ期原发性高血压患者、19例Ⅱ期和Ⅲ期原发性高血压患者以及11例肾性高血压患者（慢性肾小球肾炎和慢性肾盂肾炎），在急性失盐（速尿）刺激下以及在盐水输注急性抑制下，测定血浆醛固酮、血浆肾素活性、血浆和尿液中的钠和钾。大多数Ⅰ期原发性高血压患者在急性盐缺失时血浆醛固酮和血浆肾素活性有良好的刺激反应。40例Ⅰ期原发性高血压患者中有3例，19例Ⅱ期和Ⅲ期原发性高血压患者中有13例未表现出任何肾素分泌的刺激反应（“低肾素性高血压”）。在所有这些患者中，血浆醛固酮刺激反应保持完好。输注盐水后，所有组的血浆醛固酮和血浆肾素活性均受到抑制。血浆肾素活性的良好刺激表明，在我们的实验中，肾素-血管紧张素系统不可能是盐缺失时醛固酮分泌增加的原因。尽管肾素活性固定，但血浆醛固酮的增加很可能是由利尿剂导致的钠缺失所刺激。在所有原发性高血压患者中，我们未发现输注盐水时醛固酮分泌反应不足。肾性高血压患者血浆肾素活性的刺激和抑制反应最小。钠缺失时血浆醛固酮分泌仅略有增加，输注盐水时的降低在统计学上无显著意义。因此我们得出结论，这些患者在输注盐水和失盐时血浆醛固酮和肾素分泌反应不足。
