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Activation of the aldosterone/mineralocorticoid receptor system and protective effects of mineralocorticoid receptor antagonism in retinal ischemia-reperfusion injury.
Exp Eye Res. 2012 Mar; 96(1):116-23.EE

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.

Authors+Show Affiliations

Department of Ophthalmology, Kagawa University Faculty of Medicine, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

22200488

Citation

Liu, Ye, et al. "Activation of the Aldosterone/mineralocorticoid Receptor System and Protective Effects of Mineralocorticoid Receptor Antagonism in Retinal Ischemia-reperfusion Injury." Experimental Eye Research, vol. 96, no. 1, 2012, pp. 116-23.
Liu Y, Hirooka K, Nishiyama A, et al. Activation of the aldosterone/mineralocorticoid receptor system and protective effects of mineralocorticoid receptor antagonism in retinal ischemia-reperfusion injury. Exp Eye Res. 2012;96(1):116-23.
Liu, Y., Hirooka, K., Nishiyama, A., Lei, B., Nakamura, T., Itano, T., Fujita, T., Zhang, J., & Shiraga, F. (2012). Activation of the aldosterone/mineralocorticoid receptor system and protective effects of mineralocorticoid receptor antagonism in retinal ischemia-reperfusion injury. Experimental Eye Research, 96(1), 116-23. https://doi.org/10.1016/j.exer.2011.12.012
Liu Y, et al. Activation of the Aldosterone/mineralocorticoid Receptor System and Protective Effects of Mineralocorticoid Receptor Antagonism in Retinal Ischemia-reperfusion Injury. Exp Eye Res. 2012;96(1):116-23. PubMed PMID: 22200488.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of the aldosterone/mineralocorticoid receptor system and protective effects of mineralocorticoid receptor antagonism in retinal ischemia-reperfusion injury. AU - Liu,Ye, AU - Hirooka,Kazuyuki, AU - Nishiyama,Akira, AU - Lei,Bai, AU - Nakamura,Takehiro, AU - Itano,Toshifumi, AU - Fujita,Tomoyoshi, AU - Zhang,Jinsong, AU - Shiraga,Fumio, Y1 - 2011/12/20/ PY - 2011/07/11/received PY - 2011/11/25/revised PY - 2011/12/12/accepted PY - 2011/12/28/entrez PY - 2011/12/28/pubmed PY - 2012/5/12/medline SP - 116 EP - 23 JF - Experimental eye research JO - Exp Eye Res VL - 96 IS - 1 N2 - 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. SN - 1096-0007 UR - https://www.unboundmedicine.com/medline/citation/22200488/Activation_of_the_aldosterone/mineralocorticoid_receptor_system_and_protective_effects_of_mineralocorticoid_receptor_antagonism_in_retinal_ischemia_reperfusion_injury_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(11)00409-X DB - PRIME DP - Unbound Medicine ER -