Lack of influence of renin-angiotensin system on diabetic renal vasoconstriction

Previous study (Ha H and Dunham EW: Limited capacity for renal vasodilatation in anesthetized diabetic rats. American Journal of Physiology 1987; 253: H845-55) suggested that changes of renal vascular structure associated with diabetes could not be sole pathogenesis for decreased renal blood flow in streptozotocin-induced diabetic rats (STZR). Basal values of total renal blood flow (using an electromagnetic flowmeter), mean arterial pressure and renal vascular resistance of anesthetized STZR (n = 10) and age-matched control rats (CR; n = 9) were 6.1 ± 0.4 vs. 7.5 ± 0.5 ml min^-1 gKw^-1 (p < 0.05), 118 ± 3 vs. 114 ± 3 mmHg, and 20.1 ± 1.4 vs. 15.6 ± 0.9 mmHg ml^-1 min gKw (p < 0.01), respectively. This study evaluated the participation of the renin-angiotensin system on renal vasoconstriction of streptozotocin-induced diabetic rats (STZR) by determining the renal vascular reactivity to exogenous angiotensin (Ang) I and Ang II, and by determining the effect of captopril on renal vascular tone. The renal vascular response to intravenous Ang I (50-200 ng kg^-1) in the presence of endogenous converting enzyme activity or Ang II (4-128 ng kg^-1) in absence of that was quite similar between two groups. Captopril at 0.5 mg kg^-1 followed by 10 μg kg^-1 min^-1 produced similar degree of renal vasodilatation between STZR and age-matched control rats (CR), that is, captopril could not normalize the highered basal renal vascular resistance in STZR. In addition, chronic administration of captopril, 100 mg L^-1 of drinking water, did not prevent renal hypoperfusion associated with diabetes. These data suggest that factor(s) other than the renin-angiotensin system may play a role in renal vasoconstriction of short-term diabetic rats.