Guidi E, Giglioni A, Cozzi M G, Minetti E E
Centro di Ricerca Clinica in Nefrologia e Ipertensine Arteriosa Unità Operativa di Nefrologia Dialisi e Trapianto, Milano, Italy.
Ren Fail. 1998 Mar;20(2):243-8. doi: 10.3109/08860229809045108.
It is believed that angiotensin converting-enzyme (ACE) inhibitors lower proteinuria by acting on glomerular hemodynamics. This hypothesis predicts that the urinary excretion of a tubular protein should be unaffected by ACE inhibition. In the present study we have compared the excretion of albumin and Tamm-Horsfall Glycoprotein (THGP), a protein secreted only by renal tubules, before and after ACE inhibition. Urinary protein excretion was measured with the Phast System, a method based on SDS polyacrylamide gel electrophoresis followed by silver staining, in 15 essential hypertensives, after at least 4 weeks of wash-out from any drug and after 2 months of ACE inhibition with oral Quinapril. After 2 months of ACE inhibition, blood pressure (BP), body weight, urinary output, heart rate, plasma glucose, plasma and urinary creatinine, urate and electrolytes, and creatinine clearance, were not different from baseline values. Plasma ACE activity decreased from 76 +/- 7 to 10 +/- 4 U/mL (mean +/- SEM, 2 tails paired t test, p = 0.0001). Both albumin and THP urinary excretions decreased from 51 +/- 6 to 43 +/- 4 mg/ 24 h (p = 0.05) and from 19 +/- 3 to 12 +/- 1 mg/24 h (p = 0.02), respectively. This unexpected result suggests that ACE inhibitors may act also at the level of renal tubular cells.
人们认为，血管紧张素转换酶（ACE）抑制剂通过作用于肾小球血流动力学来降低蛋白尿。这一假说预测，肾小管蛋白的尿排泄量应不受ACE抑制的影响。在本研究中，我们比较了ACE抑制前后白蛋白和Tamm-Horsfall糖蛋白（THGP，一种仅由肾小管分泌的蛋白）的排泄情况。在15名原发性高血压患者中，在停用任何药物至少4周后，以及在用口服喹那普利进行2个月的ACE抑制后，使用Phast系统（一种基于SDS聚丙烯酰胺凝胶电泳并随后进行银染的方法）测量尿蛋白排泄量。在进行2个月的ACE抑制后，血压（BP）、体重、尿量、心率、血浆葡萄糖、血浆和尿肌酐、尿酸和电解质以及肌酐清除率与基线值无差异。血浆ACE活性从76±7降至10±4 U/mL（均值±标准误，双侧配对t检验，p = 0.0001）。白蛋白和THP的尿排泄量分别从51±6降至43±4 mg/24 h（p = 0.05）和从19±3降至12±1 mg/24 h（p = 0.02）。这一意外结果表明，ACE抑制剂可能也作用于肾小管细胞水平。
