March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Activation of the Aldosterone/Mineralocorticoid Receptor System and Protective Effects of Mineralocorticoid Receptor Antagonism in Retinal Ischemia- Reperfusion Injury
Author Affiliations & Notes
  • Kazuyuki Hirooka
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
  • Ye Liu
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
    Ophthalmology, The Fourth Affiliated Hospital of China Medical University, Shenyang, China
  • Tomoyoshi Fujita
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
  • Fumio Shiraga
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
  • Footnotes
    Commercial Relationships  Kazuyuki Hirooka, None; Ye Liu, None; Tomoyoshi Fujita, None; Fumio Shiraga, None
  • Footnotes
    Support  Alumni Association of Faculty of Medicine, Kagawa University, No. 22-1.
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6409. doi:
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      Kazuyuki Hirooka, Ye Liu, Tomoyoshi Fujita, Fumio Shiraga; Activation of the Aldosterone/Mineralocorticoid Receptor System and Protective Effects of Mineralocorticoid Receptor Antagonism in Retinal Ischemia- Reperfusion Injury. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6409.

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

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Abstract

Purpose: : To investigate whether the mineralocorticoid receptor (MR)-aldosterone system exists within the retina and whether it can influence retinal cell death in a rat retinal ischemia-reperfusion injury model.

Methods: : Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg. Rats were treated with the angiotensin II type 1 receptor (AT1-R) antagonist (candesartan), MR antagonist (spironolactone), or aldosterone. Candesartan was administered intraperitoneally 30 min before induction of the ischemia. Aldosterone was either administered by a subcutaneous osmotic minipump 1 day before the ischemia or was injected into the vitreous space 30 min prior to the ischemia. Spironolactone was orally administered to animals on a daily basis via the use of feeding needles. At 7 days after ischemia, retinal damage was evaluated. Western blot was used to measure changes in the MR expression. Immunohistochemistry was used to examine retinal localization of MR.

Results: : Pretreatment with candesartan or spironolactone significantly inhibited retinal ischemic injury. However, there was no protective effect against retinal ischemia-reperfusion injury provided by the combined aldosterone with candesartan treatment. Additionally, pretreatment with aldosterone alone also did not provide any neuroprotective effects against retinal ischemia-reperfusion injury. When rats were treated via local administration of aldosterone in the absence of ischemia, the number of retinal ganglion cells decreased while the retinal thickness remained unchanged. MR expression peaked at 12 h after ischemia, at which time the immunohistochemical analysis detected numerous MR-positive cells in the inner retina in vehicle-treated rats. Although the renin-angiotensin-aldosterone system (RAAS) was blocked by administration of candesartan, there was an increased MR expression in the inner retina at 12 h after the ischemia.

Conclusions: : The present findings demonstrated that a local aldosterone/MR system exists in the retina. Our results also demonstrated that a MR antagonist can attenuate subsequent ischemic damage in the rat retina.

Keywords: ischemia • neuroprotection • receptors: pharmacology/physiology 
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