Renal angiotensin converting enzyme (ACE) expression in diabetic rats the effect of ACE inhibitors

Abstract

Renal excreted angiotensin converting enzyme (ACE) inhibitor captopril, and renal·hepatic bile excreted ACE inhibitor temocapril, were compared by monitoring serum ACE and renal ACE expression (protein and mRNA) in streptozotocin-induced diabetic rats. Serum ACE levels did not change in untreated diabetic rats or in those treated with temocapril, compared with normal control rats. However, serum ACE levels significantly increased in diabetic rats treated with captopril after 3 months (153.8± 23.0 vs. 43.5±5.5 IU/l/37°C, p< 0.01) and 6 months (113.6± 9.3 vs. 36.9± 2.9 IU/ l/37°C, p< 0.01) compared with normal control rats. Compared with normal control rats (3.6± 0.4), proximal tubular ACE protein expression significantly (p< 0.01) decreased in untreated diabetic rats (1.6 ± 1.1), but significantly (p< 0.01) increased in diabetic rats treated with captopril (3.7± 0.3) and temocapril (3.5± 0.4). Renal ACE mRNA levels decreased in untreated diabetic rats (125.5± 20.3 vs. 313.3± 53.4, p< 0.01) compared with normal control rats for 6 months. Renal ACE mRNA levels tended to increase in diabetic rats treated with captopril (l84.4± 51.2 vs. 125.5± 20.3) and temocapril (165.4± 43.2 vs. 125.5± 20.3) compared with untreated diabetic rats for 6 months. In conclusion, diabetic rats had lower proximal tubular ACE protein expression and lower renal ACE mRNA levels compared with normal control rats. Furthermore, both ACE inhibitors increased renal ACE nrntein and mRNA expressionn but differed in their effect on serum ACE levels.