Bönner G, Gentges A, Wambach G, Kaufmann W
Dept. of Internal Medicine II, Merheim Hospital, University of Cologne, Köln, F.R.G.
Agents Actions Suppl. 1987;22:309-19. doi: 10.1007/978-3-0348-9299-5_32.
The effect of furosemide (40 mg iv) on diuresis, natriuresis and renal kallikrein and kinin excretion was investigated without and with pretreatment by captopril (100 mg po). Furosemide stimulated markedly diuresis and natriuresis as well as urinary kallikrein and kinin excretion. Pretreatment by captopril (C) reduced the diuretic and natriuretic effect of furosemide significantly (UNaV pre-C: +15, 1 +/- 2.1 ml/min vs. post-C: 7.0 +/- 0.3 ml/min; p less than 0.001). Similar changes in urinary kallikrein and kinin excretion were observed after captopril pretreatment, but because of the great coefficient of variation these changes did not reach statistical significance. The reason for the reduced activity of furosemide after captopril pretreatment was the diminished proximal-tubular secretion of furosemide, as it could be shown by direct measurement of the drug in urine. After furosemide injection changes in plasma aldosterone concentration paralleled changes in renal kallikrein and kinin excretion. However, after captopril there was a sharp dissociation between aldosterone, which was diminished by captopril continuously, and renal kallikrein and kinins, which were still stimulated by furosemide. These results suggest that renal kallikrein-kinin system is stimulated by furosemide directly and independently of aldosterone secretion.
研究了呋塞米（静脉注射40毫克）在未用卡托普利（口服100毫克）预处理和预处理后的情况下对利尿、利钠以及肾脏激肽释放酶和激肽排泄的影响。呋塞米显著刺激了利尿、利钠以及尿激肽释放酶和激肽的排泄。卡托普利预处理降低了呋塞米的利尿和利钠作用（卡托普利预处理前尿钠排泄量：+15.1±2.1毫升/分钟，卡托普利预处理后：7.0±0.3毫升/分钟；p＜0.001）。卡托普利预处理后观察到尿激肽释放酶和激肽排泄有类似变化，但由于变异系数较大，这些变化未达到统计学显著性。卡托普利预处理后呋塞米活性降低的原因是呋塞米近端小管分泌减少，这可通过直接测量尿中药物得以证实。注射呋塞米后，血浆醛固酮浓度的变化与肾脏激肽释放酶和激肽排泄的变化平行。然而，卡托普利治疗后，醛固酮（持续被卡托普利降低）与肾脏激肽释放酶和激肽（仍受呋塞米刺激）之间出现了明显分离。这些结果表明，肾脏激肽释放酶-激肽系统受呋塞米直接刺激，且独立于醛固酮分泌。
