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Michel Lonchampt, Laurence Pennel, Jacques Duhault; Hyperoxia/Normoxia-Driven Retinal Angiogenesis in Mice: A Role for Angiotensin II. Invest. Ophthalmol. Vis. Sci. 2001;42(2):429-432.
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purpose. To examine a possible role for the angiotensin system in a rodent model
of retinopathy of prematurity.
methods. A previously described model was used in which oxygen cycling (5 days
hyperoxia and 5 days hypoxia) induced retinal alterations in newborn
mice. An angiotensin-converting enzyme inhibitor (perindopril), or
angiotensin receptor antagonists AT1 (losartan) or AT2 (PD123319) were
administered subcutaneously for 5 days after the hyperoxia exposure.
According to histologic methods, the endothelial cell count within the
anterior part of the ganglion cell layer was used for the evaluation of
the compound effect.
results. Histologic evaluation showed an increased number of endothelial cells
in retinas of hypoxic pups compared with hyperoxic or normoxic pups.
Hypoxic animals treated with perindopril (4 mg/kg) showed a significant
decrease (29%, P ≤ 0.001) in endothelial cell
number (163 ± 7) compared with hypoxic control animals (231 ± 10). Losartan also decreased the endothelial cell number (14%, P ≤ 0.05), whereas the AT2 antagonist had no
conclusions. The data showed a protective effect of an angiotensin-converting enzyme
inhibitor and of an AT1 receptor antagonist on hyperoxia- and
normoxia-induced neovascularization in newborn mice. The results
suggest a role for the angiotensin system in this model and that such
compounds may be of interest in the prevention of proliferative
retinopathies such as proliferative diabetic
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