Cooper M E, Allen T J, Macmillan P, Bach L, Jerums G, Doyle A E
Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria.
Am J Hypertens. 1988 Jan;1(1):5-10. doi: 10.1093/ajh/1.1.5.
To evaluate whether hypertension is a cause or just an association with diabetic renal disease, diabetes was induced in both normotensive Wistar-Kyoto and spontaneously hypertensive rats (WKY and SHR). Animals were assessed monthly for 8 months before sacrifice. When compared to normotensive diabetic rats (WKY-STZ), hypertensive diabetic rats (SHR-STZ) had an earlier and more rapid rise in urinary albumin excretion. In addition, SHR-STZ had increased glomerular basement membrane thickness when compared to WKY-STZ or SHR. In a separate experiment, Enalapril therapy (35 mg/L) was administered in drinking water to WKY-STZ and SHR-STZ. Enalapril significantly reduced blood pressure in both animal groups, and this was associated with a decrease in urinary albumin excretion. The SHR-STZ model has accelerated nephropathy as determined by both functional and structural parameters. Angiotensin-converting enzyme inhibition is associated with a reduction in albuminuria in both hypertensive and normotensive models of diabetic nephropathy.
为评估高血压是糖尿病肾病的病因还是仅仅与之相关，在正常血压的Wistar-Kyoto大鼠和自发性高血压大鼠（WKY和SHR）中诱导糖尿病。在处死前每月对动物进行评估，持续8个月。与正常血压的糖尿病大鼠（WKY-STZ）相比，高血压糖尿病大鼠（SHR-STZ）尿白蛋白排泄量升高更早且更快。此外，与WKY-STZ或SHR相比，SHR-STZ的肾小球基底膜厚度增加。在另一项实验中，给WKY-STZ和SHR-STZ的饮用水中加入依那普利治疗（35mg/L）。依那普利显著降低了两组动物的血压，且这与尿白蛋白排泄量减少相关。根据功能和结构参数测定，SHR-STZ模型存在加速性肾病。在高血压和正常血压的糖尿病肾病模型中，血管紧张素转换酶抑制均与蛋白尿减少相关。
