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Should the use of short acting angiotensin-converting enzyme inhibitors be abandoned?

Institute of Hypertension and Kidney Diseases, Rabin Medical Center (Beilinson Campus) Petah Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel

Geoffrey Boner

Institute of Hypertension and Kidney Diseases, Rabin Medical Center (Beilinson Campus) Petah Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel, gboner@ clalit.org.il

David J van Dijk

Institute of Hypertension and Kidney Diseases, Rabin Medical Center (Beilinson Campus) Petah Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel

Background Angiotensin-converting enzyme inhibitors (ACE-I) have different modes of action and different durations of inhibition. The effects of ACE-I on the various components of the renin-angiotensin system (RAS) at trough hours were studied in patients with diabetes mellitus receiving long-term ACE-I treatment.

Methods Out of 86 Type 1 and 2 diabetic patients, 49 were untreated, 25 received captopril and 12 received enalapril as chronic treatment. Blood for the determination of plasma renin activity (PRA), serum ACE activity and plasma angiotensin II (Ang II) was drawn in the morning (0700—0900 hours) after an overnight fast, about 12 hours after the last dose. PRA and Ang II were measured by RIA and serum ACE activity was assayed by a radiometric assay using ³H-hippuryl-glycyl-glycine as a substrate.

Results Mean age was significantly greater in the enalapril-treated patients. Systolic and diastolic blood pressures were not different between the captopril-treated and untreated groups. Serum ACE activity in the captopril-treated diabetic patients was 101.5±42.5 nmol/mL/min, values obtained in untreated diabetic patients (101.4±25.2 nmol/mL/min). In contrast, ACE activity in the enalapril-treated patients was significantly reduced (5.5±7.5 nmol/mL/min) compared with untreated and captopril-treated patients (p<0.00001). PRA values in the ACE-I treated patients were significantly increased. Plasma Ang II levels were significantly increased in the captopril-treated vs. untreated patients (65.1±50.2 vs. 36.2±31.7 pg/mL, p=0.006), whereas the values in the enalapril-treated patient were slightly, but not significantly, reduced (23.8±21.4 pg/mL).

Conclusion Trough serum ACE activity is not suppressed in diabetic patients receiving captopril, compared with those receiving enalapril and we thus question the use of short acting ACE-I in these patients.

Key Words: ACE • ACE inhibitors • angiotensin • diabetes mellitus

Journal of Renin-Angiotensin-Aldosterone System, Vol. 1, No. 4, 365-368 (2000)
DOI: 10.3317/jraas.2000.068


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