Risler T, Erley C M
Sektion Nieren- und Hochdruckkrankheiten, Universität Tübingen.
Z Kardiol. 1993;82 Suppl 4:39-44.
A considerable number of hormones control renal perfusion to preserve glomerular filtration. We used the "captopril test" to characterize patients with renal-vascular hypertension. This study revealed a group of patients which reacted to 25 mg of captopril with a significant increase of plasma renin activity, but angiography excluded a renal artery stenosis. These patients had significantly more hypertensive organ damage than a control-group, including a significant microalbuminuria. Consequently, we infused a subpressure dose of angiotensin II to investigate its impact on albuminuria in these patients. Although angiotensin II induced hyperfiltration, microalbuminuria was not increased. Because this finding could have therapeutic relevance, we investigated the significance of different antihypertensive drugs (beta-blocker, alpha-blocker, Calcium antagonists, ACE-inhibitor) on microalbuminuria in patients with arterial hypertension. Renal hemodynamics were influenced as expected, but blood-pressure and microalbuminuria were reduced to the same extent by all antihypertensives. In contrast to these results, we could demonstrate significantly different influences of a beta-blocker and an ACE-inhibitor on proteinuria in patients with primary glomerulonephritis. These results suggest different effects of antihypertensive drugs on renal protein excretion depending on the actual disease.
相当数量的激素控制肾脏灌注以维持肾小球滤过。我们使用“卡托普利试验”来对肾血管性高血压患者进行特征描述。这项研究发现一组患者，他们对25毫克卡托普利的反应是血浆肾素活性显著增加，但血管造影排除了肾动脉狭窄。这些患者的高血压性器官损害明显多于对照组，包括明显的微量白蛋白尿。因此，我们输注了低于正常压力剂量的血管紧张素II，以研究其对这些患者白蛋白尿的影响。尽管血管紧张素II诱导了超滤，但微量白蛋白尿并未增加。由于这一发现可能具有治疗意义，我们研究了不同降压药物（β受体阻滞剂、α受体阻滞剂、钙拮抗剂、ACE抑制剂）对动脉高血压患者微量白蛋白尿的影响。肾脏血流动力学受到了预期的影响，但所有降压药都使血压和微量白蛋白尿降低到相同程度。与这些结果相反，我们可以证明β受体阻滞剂和ACE抑制剂对原发性肾小球肾炎患者蛋白尿有显著不同的影响。这些结果表明，降压药物对肾脏蛋白质排泄的影响因实际疾病而异。
