Abstract

The purpose of this project was to investigate the effects of the mineralocorticoid receptor antagonist against retinal ischemia-reperfusion injury and identify the aldosterone/mineralocorticoid receptor (MR) system in the rat retina. Retinal ischemia was induced by increasing intraocular pressure to 130 mmHg. Rats were treated with the angiotensin II type 1 receptor (AT1-R) antagonist (candesartan), MR antagonist (spironolactone), or aldosterone. Retinal damage was evaluated at 7 days after the ischemia by measuring the retinal thickness and the number of retinal ganglion cells. Pretreatment with candesartan, spironolactone, or candesartan and 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. The present findings demonstrated the existence of a local aldosterone/MR system in the retina. Our results also demonstrated that an MR antagonist can attenuate subsequent ischemic damage in the rat retina.

Links

Publisher Full Text

Authors

Liu Y, Hirooka K, Nishiyama A, Lei B, Nakamura T, Itano T, Fujita T, Zhang J, Shiraga F

Institution

Department of Ophthalmology, Kagawa University Faculty of Medicine, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan.

Source

Experimental eye research 96:1 2012 Mar pg 116-23

MeSH

Aldosterone
Aldosterone Antagonists
Angiotensin II Type 1 Receptor Blockers
Animals
Benzimidazoles
Cell Survival
Male
Rats
Rats, Sprague-Dawley
Receptors, Mineralocorticoid
Renin-Angiotensin System
Reperfusion Injury
Retinal Diseases
Spironolactone
Tetrazoles

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22200488