Key result
ACE inhibition improved neovascularization in the diabetic ischemic leg (angiographic score increased 2.7-fold, P<0.01) but reduced vessel growth in the diabetic retina.
Why the study?
Does ACE inhibition or AT1 receptor blockade improve angiogenesis in ischemic limbs and reduce retinal neovascularization in type 1 diabetic mice?
Population
Type 1 diabetic mice, including bradykinin B2 receptor-deficient animals, subjected to hind limb ischemia.
Comparison
ACE inhibitor or AT1 receptor blocker for 4… vs Untreated diabetic mice and nondiabetic mice.
Design
Preclinical
Follow-up
5 months
Authors
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ACE inhibition may exert tissue-specific angiogenic effects in diabetic models; leaves open translation to human limb or retinal disease.
Does ACE inhibition or AT1 receptor blockade improve angiogenesis in ischemic limbs and reduce retinal neovascularization in type 1 diabetic mice?
Effect estimate: 2.7-fold, 2.0-fold, and 1.6-fold increase
p-value: p=<0.01
ACE inhibition exerts a dual effect in diabetic mice, improving ischemia-induced neovascularization in the leg via bradykinin signaling while reducing pathological vessel growth in the retina by inhibiting the Ang II pathway.
Ebrahimian et al. (2004) studied Type 1 Diabetes with hind limb ischemia. ACEI (Perindopril) or AT1 receptor blocker (Candesartan) vs. Untreated diabetic animals was evaluated on Angiographic score, capillary density, and foot perfusion in ischemic leg (2.7-fold, 2.0-fold, and 1.6-fold increase, p=<0.01). ACE inhibition improved neovascularization in the diabetic ischemic leg (angiographic score increased 2.7-fold, P<0.01) but reduced vessel growth in the diabetic retina.
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