1. Diabetes mellitus was induced by streptozotocin in male Wistar rats, and angiotensin‐converting enzyme measured in plasma and mesenteric vessels 3 weeks later. 2. Diabetes was associated with increased mesenteric wet weight/ bodyweight ratio (control 0.2 s.e.m. 0.02 mg/g, n= 21, vs diabetes 1.0 s.e.m. 0.3 mg/g, n= 27, P < 0.01, ANOVA). 3. Plasma angiotensin‐converting enzyme activity was increased in diabetic rats (98 s.e.m. 3 nmol HL/mL per min) compared with controls (64 s.e.m. 6 nmol HL/mL per min, P < 0.01, ANOVA). 4. Mesenteric vessel angiotensin‐converting enzyme was increased in diabetes mellitus estimated by radioligand binding site density (fmol/mg protein; 1407 s.e.m. 166 fmol/mg protein) compared with controls (890 s.e.m. 56 fmol/mg protein, P < 0.05, ANOVA) and by enzyme kinetic assay (diabetes, 15.5 s.e.m. 1.5 nmol HL/mg protein per min, controls, 8.3 s.e.m. 0.7 nmol HL/mg protein per min, P < 0.01, ANOVA). The equilibrium dissociation constant of ligand‐angiotensin‐converting enzyme interaction was unchanged. 5. Increased vascular angiotensin‐converting enzyme concentration may contribute to vascular hypertrophy and diabetic vasculopathy by increased local synthesis of angiotensin II.
|Number of pages||5|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - May 1992|
- blood vessels
- diabetes mellitus
- renin‐angiotensin system.