May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Inhibitory Effect of Retinal and Choriodal Neovascularization by Candesartan
Author Affiliations & Notes
  • E. Yamada
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
  • H. Yamada
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
  • A. Higuchi
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
  • M. Matsumura
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
  • Footnotes
    Commercial Relationships  E. Yamada, None; H. Yamada, None; A. Higuchi, None; M. Matsumura, None.
  • Footnotes
    Support  Grant supported by JSPS
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 553. doi:
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      E. Yamada, H. Yamada, A. Higuchi, M. Matsumura; Inhibitory Effect of Retinal and Choriodal Neovascularization by Candesartan . Invest. Ophthalmol. Vis. Sci. 2003;44(13):553.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Angiotensin converting Enzyme Inhibitor (ACE-I) and Angiotensin II receptor-1 blocker (ARB) are commonly used for treatment of hypertension. Their clinical advantages include a reduction in blood pressure and improved prognosis in patients suffering cardiac or cerebral infarction via a vascular remodeling effect. Recently, there have been reports describing the anti-neovascular effect of ACE-I. We studied the efficacy of Candesartan, an ARB, on choroidal neovascularization (CNV). Methods: To induce retinal NV by hypoxic retinopathy, C57bl mice were kept under 75% oxygen for 5 days from P7 to P12, then moved to a normal environment for 5 days. These animals were given 1, 10mg/kg Candesartan or vehicle once a day for 5 days. Animals were sacrificed at P17 and perfused with fluorescein dextran via the left ventricle before enucleation, or enucleated immediately and prepared for sectioning. Fluorescein-dextran-perfused eyeballs were fixed in buffered formallin. Retinae were dissected, flat mounted on slide glass, and observed under a fluorescence microscope. Non-perfused areas (NPAs) were evaluated using ImagePro Plus software. Cryo-sectioned eyeballs were stained immunohistochemically by gliffonia simpliciforia isolectin-B4 and the NV beneath the retina were evaluated. To induce experimental CNV, adult C57bl mice were anesthetized and exposed to Krypton laser in order to break Bruch's membrane. After laser treatment, we administered 10mg/kg Candesartan or vehicle only once a day for 14 days. At day 14, eyeballs were enucleated and fixed in formallin Under a dissection microscope, the posterior portion of the eye balls were isolated, mounted choroidal side up and observed by fluorescence microscopy. Using ImagePro PlusSoftware, the areas of CNV were evaluated. Results: Mice given 10mg/kg Candesartan showed less retinal NV than those receiving vehicle only. The size of NPA showed no statistical difference between Candesartan and vehicle only. The size of CNV was statistically smaller in Candesartan than that of mice given vehicle only. Conclusions: Like ACE-I, ARB suppressed ocular NV by blocking the effect of angiotensin II. This suggests that angiotensin II acts as a stimulus of ocular neovascularization.

Keywords: retinal neovascularization • choroid: neovascularization • drug toxicity/drug effects 

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