Pathogenetic Role of Renal ACE Activity and Angiotensin-II in Development of Microalbuminuria in Patients with NIDDM.
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Blood and urinary ACE activity (colorimetry) and angiotensin-II (AG-II, RIA) levels were determined before and after infusion of L-arginine (LA), which inhibits tubular reabsorption of proteins, in 48 NIDDM patients with (NIDDM-II, N =22) or without microalbuminuria (MAU)(NIDDM-I, N =26) and in healthy controls (N =20) to elucidate the pathogenetic role of renal AG-II in the development of MAU. LA induced 2-to 4-fold increases in urinary ACE activity and AG-II, while it did not influence blood ACE activity and AG-II in all groups. No differences were found in blood ACE activity and AG-II among the three subject groups. On the other hand, urinary ACE activity (27.1±2.5→65.7±5.1 mIU/hr) and AG-II (20.8±3.4→74.1±5.8 ng/hr) in the NIDDM-II group were the highest, and those in the NIDDM-I group (ACE: 19.0±2.2→49.9 ± 3.4 mIU/hr, AG-II: 16.8±3.5 →56.5±6.3 ng/hr) were higher than in the controls (ACE: 13.9±2.6 →38.4±3.5 mIU/hr, AG-II: 11.4±2.6→37.9±3.9 ng/hr). In the group as a whole, urinary ACE activity and AG-II were correlated with AER and glomerular filtration of albumin, and inversely correlated with the rate of tubular reabsorption of albumin before and after LA, the stronger correlations being found after LA (ACE: r=0.40 vs AER, r=0.47 vs GCA, r=-0.39 vs TRRA, AG-II: r=0.50 vs AER, r=0.46 vs GCA, r=-0.54 vs TRRA). On the other hand, blood ACE activity and AG-II did not have a significant correlation with either of them (r=-0.22-0.13). These results indicate that renal AG-II, produced by ACE, plays a permissive role in the development of MAU in NIDDM.
- 一般社団法人 日本糖尿病学会の論文
一般社団法人 日本糖尿病学会 | 論文
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