Jenkins D A, Cowan P, Collier A, Watson M L, Clarke B F
Diabetic Department, University Department of Medicine, Edinburgh Royal Infirmary, UK.
Diabet Med. 1990 Mar-Apr;7(3):252-7. doi: 10.1111/j.1464-5491.1990.tb01380.x.
Elevation of glomerular filtration rate (GFR) is a feature of diabetes mellitus in humans and in animal models. Angiotensin II has been implicated as a mediator of GFR in diabetes. The acute effect of inhibition of angiotensin converting enzyme with captopril on renal haemodynamic and endocrine parameters was therefore studied in 14 normotensive male Type 1 diabetic patients, and the responses compared with those in five normal male control subjects. Following captopril 12.5 mg orally the diabetic patients exhibited an acute fall in GFR from 122 +/- 3.8 to 113 +/- 4.5 ml min-1 1.73-m-2 (p less than 0.02) and a rise in renal plasma flow (RPF) from 670 +/- 57 to 797 +/- 46 ml min-1 1.73-m-2 (p less than 0.01) which resulted in a fall in filtration. This did not occur in normal control subjects. Natriuresis occurred only in normal control subjects. There was no change in urinary excretion of PGE2 or kallikrein in either group but excretion of 6-keto-PGF1 alpha fell in the diabetic patients. There was a significant correlation between glycosylated haemoglobin and baseline RPF (rs = -0.79, p less than 0.001) and filtration fraction (rs = 0.83, p less than 0.001) that persisted when the change in these variables following captopril was analysed. Our results are compatible with the response to ACE inhibition in diabetic patients being secondary to inhibition of angiotensin II and suggest that this response may be related to blood glucose control.
肾小球滤过率（GFR）升高是人类和动物糖尿病模型的一个特征。血管紧张素II被认为是糖尿病中GFR的介导因子。因此，研究了卡托普利抑制血管紧张素转换酶对14名血压正常的1型糖尿病男性患者肾脏血流动力学和内分泌参数的急性影响，并将其反应与5名正常男性对照受试者进行了比较。口服12.5mg卡托普利后，糖尿病患者的GFR从122±3.8降至113±4.5ml·min-1·1.73-m-2（p<0.02），肾血浆流量（RPF）从670±57升至797±46ml·min-1·1.73-m-2（p<0.01），导致滤过率下降。正常对照受试者未出现这种情况。利钠作用仅发生在正常对照受试者中。两组患者的PGE2或激肽释放酶尿排泄量均无变化，但糖尿病患者的6-酮-PGF1α排泄量下降。糖化血红蛋白与基线RPF（rs=-0.79，p<0.001）和滤过分数（rs=0.83，p<0.001）之间存在显著相关性，在分析卡托普利后这些变量的变化时，这种相关性仍然存在。我们的结果与糖尿病患者对ACE抑制的反应继发于血管紧张素II抑制的观点一致，并表明这种反应可能与血糖控制有关。
