Key result
Exogenous administration of Angiotensin-(1-7) significantly reversed streptozotocin-induced renal hypertrophy in diabetic rats, reducing the kidney weight/body weight ratio from 0.50 to 0.379 (p<0.05).
Why the study?
Does exogenous angiotensin-(1-7) reduce renal hypertrophy in rats with streptozotocin-induced diabetes mellitus?
Does exogenous angiotensin-(1-7) reduce renal hypertrophy in rats with streptozotocin-induced diabetes mellitus?
Absolute Event Rate: 0.379% vs 0.5%
p-value: p=<0.05
Exogenous administration of angiotensin-(1-7) attenuates early renal hypertrophy and improves renal function in a rat model of streptozotocin-induced diabetes.
Hypothesis-generating for angiotensin-(1-7) in diabetic nephropathy; clinical translation remains untested.
Participation of angiotensin II in chronic kidney diseases including diabetic nephropathy (DN) has been extensively described. Similarly, several studies support a protective role for angiotensin-(1-7). However, other studies suggest that some of the cellular effects of angiotensin-(1-7) may be deleterious. The objective of this study was to determine the role of exogenous angiotensin-(1-7) on renal hypertrophy development in rats with streptozotocin-induced diabetes. A control group and three groups of rats with streptozotocin-induced diabetes: untreated diabetic rats, diabetic rats treated with captopril, and diabetic rats treated with angiotensin-(1-7), were studied. After two weeks of treatment, the kidneys were removed under anesthesia with pentobarbital. The kidneys were weighed and the renal cortex was separated for analysis of AT1R, TGF-β1, MASR, and ACE2 expression by western blot. Rats in the three groups with diabetes had hyperglycemia, increased food and water consumption, and higher urinary volume than control rats. Treatment with captopril or angiotensin-(1-7) reversed streptozotocin-induced renal hypertrophy, measured by kidney weight, protein/DNA ratio in renal cortex, glomerular area, or proximal tubular cells area, proteinuria, and creatinine clearance reduction. AT1R, TGF-β1, and MAS receptor expression in renal cortex of diabetic rats increased significantly as compared to controls (p
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Amato et al. (2016) studied Streptozotocin-induced diabetes mellitus (diabetic nephropathy) (n=20). Angiotensin-(1-7) vs. Untreated diabetic rats (vehicle) and captopril was evaluated on Kidney weight/body weight ratio (p=<0.05). Exogenous administration of Angiotensin-(1-7) significantly reversed streptozotocin-induced renal hypertrophy in diabetic rats, reducing the kidney weight/body weight ratio from 0.50 to 0.379 (p<0.05).
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