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Neuroprotection against retinal ischemia-reperfusion injury by blocking the angiotensin II type 1 receptor.
Invest Ophthalmol Vis Sci. 2010 Jul; 51(7):3629-38.IO

Abstract

PURPOSE.

To investigate the effects of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II antagonist against retinal ischemia-reperfusion injury in the rat retina.

METHODS.

Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg. Rats were treated with an ACE inhibitor (captopril), an angiotensin II type 1 receptor (AT1-R) antagonist (candesartan), an AT2-R antagonist (PD123319), bradykinin, or a bradykinin B2 receptor antagonist (icatibant). At 7 days after the ischemia, retinal damage was evaluated. Immunohistochemistry and image analysis were used to measure changes in the levels of reactive oxygen species (ROS) and the localization of AT1-R. Dark-adapted full-field electroretinography (ERG) was also performed.

RESULTS.

Pretreatment with captopril or candesartan significantly inhibited the ischemic injury of the inner retina. However, PD123319, bradykinin, or icatibant did not reduce the ischemic damage. In control retinas, retinal vessels were positive for AT1-R. In contrast, 12 hours after ischemia, immunohistochemical analysis detected numerous AT1-R-positive cells in the inner retina in vehicle-treated rats. After ischemia, the production of ROS was detected in retinal cells. However, pretreatment with captopril or candesartan suppressed the production of ROS. On the seventh postoperative day, the amplitudes of the ERG b-waves were significantly lower in the vehicle group than in the groups pretreated with captopril or candesartan.

CONCLUSIONS.

The present findings demonstrate that ischemic damage promotes the expression of AT1-R in the inner retina. Both the ACE inhibitor and the AT1-R antagonist that were examined can block the stimulation of the AT1-R and attenuate the subsequent ischemic damage in the rat retina.

Authors+Show Affiliations

Departments of Ophthalmology, Kagawa University Faculty of Medicine, Kagawa, Japan. snipeman@med.kagawa-u.ac.jpNo 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

20164447

Citation

Fukuda, Kouki, et al. "Neuroprotection Against Retinal Ischemia-reperfusion Injury By Blocking the Angiotensin II Type 1 Receptor." Investigative Ophthalmology & Visual Science, vol. 51, no. 7, 2010, pp. 3629-38.
Fukuda K, Hirooka K, Mizote M, et al. Neuroprotection against retinal ischemia-reperfusion injury by blocking the angiotensin II type 1 receptor. Invest Ophthalmol Vis Sci. 2010;51(7):3629-38.
Fukuda, K., Hirooka, K., Mizote, M., Nakamura, T., Itano, T., & Shiraga, F. (2010). Neuroprotection against retinal ischemia-reperfusion injury by blocking the angiotensin II type 1 receptor. Investigative Ophthalmology & Visual Science, 51(7), 3629-38. https://doi.org/10.1167/iovs.09-4107
Fukuda K, et al. Neuroprotection Against Retinal Ischemia-reperfusion Injury By Blocking the Angiotensin II Type 1 Receptor. Invest Ophthalmol Vis Sci. 2010;51(7):3629-38. PubMed PMID: 20164447.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotection against retinal ischemia-reperfusion injury by blocking the angiotensin II type 1 receptor. AU - Fukuda,Kouki, AU - Hirooka,Kazuyuki, AU - Mizote,Masanori, AU - Nakamura,Takehiro, AU - Itano,Toshifumi, AU - Shiraga,Fumio, Y1 - 2010/02/17/ PY - 2010/2/19/entrez PY - 2010/2/19/pubmed PY - 2010/8/3/medline SP - 3629 EP - 38 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 51 IS - 7 N2 - PURPOSE. To investigate the effects of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II antagonist against retinal ischemia-reperfusion injury in the rat retina. METHODS. Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg. Rats were treated with an ACE inhibitor (captopril), an angiotensin II type 1 receptor (AT1-R) antagonist (candesartan), an AT2-R antagonist (PD123319), bradykinin, or a bradykinin B2 receptor antagonist (icatibant). At 7 days after the ischemia, retinal damage was evaluated. Immunohistochemistry and image analysis were used to measure changes in the levels of reactive oxygen species (ROS) and the localization of AT1-R. Dark-adapted full-field electroretinography (ERG) was also performed. RESULTS. Pretreatment with captopril or candesartan significantly inhibited the ischemic injury of the inner retina. However, PD123319, bradykinin, or icatibant did not reduce the ischemic damage. In control retinas, retinal vessels were positive for AT1-R. In contrast, 12 hours after ischemia, immunohistochemical analysis detected numerous AT1-R-positive cells in the inner retina in vehicle-treated rats. After ischemia, the production of ROS was detected in retinal cells. However, pretreatment with captopril or candesartan suppressed the production of ROS. On the seventh postoperative day, the amplitudes of the ERG b-waves were significantly lower in the vehicle group than in the groups pretreated with captopril or candesartan. CONCLUSIONS. The present findings demonstrate that ischemic damage promotes the expression of AT1-R in the inner retina. Both the ACE inhibitor and the AT1-R antagonist that were examined can block the stimulation of the AT1-R and attenuate the subsequent ischemic damage in the rat retina. SN - 1552-5783 UR - https://www.unboundmedicine.com/medline/citation/20164447/Neuroprotection_against_retinal_ischemia_reperfusion_injury_by_blocking_the_angiotensin_II_type_1_receptor_ L2 - https://iovs.arvojournals.org/article.aspx?doi=10.1167/iovs.09-4107 DB - PRIME DP - Unbound Medicine ER -