Effect of the renin inhibitor aliskiren against retinal ischemia-reperfusion injury

Kaori Tenkumo, Kazuyuki Hirooka, Shamshad J. Sherajee, Takehiro Nakamura, Toshifumi Itano, Eri Nitta, Tomoyoshi Fujita, Akira Nishiyama, Fumio Shiraga

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12 Citations (Scopus)


The purpose of this study was to investigate the effect of the renin inhibitor, aliskiren, on retinal ischemia-reperfusion injury. Retinal ischemia was induced by increasing intraocular pressure to 130mmHg. At 7 days after ischemia, retinal damage was evaluated by measuring the retinal thickness and the number of retinal ganglion cells. Western blot was used to measure changes in the (pro)renin receptor expression. Retinal mRNA expressions of prorenin, angiotensinogen and angiotensin II type 1 receptor (AT1-R) were measured by real-time polymerase chain reaction. Rats were treated with the renin inhibitor, aliskiren. Although the number of retinal ganglion cells and the inner retinal thickness were significantly decreased at 7 days after ischemia, treatment with aliskiren significantly inhibited retinal ischemic injury. Administration of aliskiren increased mRNA expression of prorenin in the retina at 3h after the reperfusion. The expression of the (pro)renin receptor was not changed after ischemia-reperfusion injury with or without aliskiren. Although there was an increase in the retinal expression of AT1-R at 3h after the reperfusion, aliskiren administration suppressed this expression. A renin inhibitor attenuated subsequent ischemic damage in the rat retina via the inhibition of the prorenin-induced angiotensin generation.

Original languageEnglish
Pages (from-to)110-118
Number of pages9
JournalExperimental Eye Research
Publication statusPublished - May 2014


  • (pro)renin
  • Aliskiren
  • Angiotensin II type 1 receptor (AT1-R)
  • Angiotensinogen
  • Renin
  • Renin-angiotensin-aldosterone-system
  • Retinal ischemia

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience


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