Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril
Hypothesis: Hyperglycemia decreases angiotensin-(1-7), the endogenous counter-regulator of angiotensin II in the retina. Materials and methods: The distribution and levels of retinal angiotensin II (Ang II) and angiotensin-(1-7) (Ang-(1-7)) were evaluated by confocal imaging and quantitative immunoh...
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Series: | Journal of the Renin-Angiotensin-Aldosterone System |
Online Access: | https://doi.org/10.1177/1470320318789323 |
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doaj-3218e07fef5d495f8267316182b73a652021-05-02T17:47:20ZengHindawi - SAGE PublishingJournal of the Renin-Angiotensin-Aldosterone System1752-89762018-08-011910.1177/1470320318789323Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captoprilPreenie deS Senanayake0Vera L Bonilha1John W Peterson2Yoshiro Yamada3Sadashiva S Karnik4Firouz Daneshgari5K Bridget Brosnihan6Joe G Hollyfield7Department of Ophthalmology, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, USADepartment of Ophthalmology, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, USAReseach Core Services (Imaging) Cleveland Clinic, Cleveland, USADepartment of Urology, Kyoto Prefectural University of Medicine, Kyoto, JapanDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, USADepartment of Urology (FD), Case Western Reserve University, University Hospitals Case Medical Center, Cleveland, USADepartment of Surgery, Hypertension & Vascular Research, Cardiovascular Sciences Center, Wake Forest University School of Medicine, Winston-Salem, USADepartment of Ophthalmology, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, USAHypothesis: Hyperglycemia decreases angiotensin-(1-7), the endogenous counter-regulator of angiotensin II in the retina. Materials and methods: The distribution and levels of retinal angiotensin II (Ang II) and angiotensin-(1-7) (Ang-(1-7)) were evaluated by confocal imaging and quantitative immunohistochemistry during the development of streptozotocin-induced diabetes in rats. Results: In the nondiabetic eye, Ang II was localized to the endfeet of Müller cells, extending into the cellular processes of the inner plexiform layer and inner nuclear layer; Ang-(1-7) showed a wider distribution, extending from the foot plates of the Müller cells to the photoreceptor layer. Eyes from diabetic animals showed a higher intensity and extent of Ang II staining compared with nondiabetic eyes, but lower intensity with a reduced distribution of Ang-(1-7) immunoreactivity. Treatment of the diabetic animals with the angiotensin-converting enzyme inhibitor (ACEI) captopril showed a reduced intensity of Ang II staining, whereas increased intensity and distribution were evident with Ang-(1-7) staining. Conclusions: These studies reveal that pharmacological inhibition with ACEIs may provide a specific intervention for the management of the diabetes-induced decline in retinal function, reversing the profile of the endogenous angiotensin peptides closer to the normal condition.https://doi.org/10.1177/1470320318789323 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Preenie deS Senanayake Vera L Bonilha John W Peterson Yoshiro Yamada Sadashiva S Karnik Firouz Daneshgari K Bridget Brosnihan Joe G Hollyfield |
spellingShingle |
Preenie deS Senanayake Vera L Bonilha John W Peterson Yoshiro Yamada Sadashiva S Karnik Firouz Daneshgari K Bridget Brosnihan Joe G Hollyfield Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril Journal of the Renin-Angiotensin-Aldosterone System |
author_facet |
Preenie deS Senanayake Vera L Bonilha John W Peterson Yoshiro Yamada Sadashiva S Karnik Firouz Daneshgari K Bridget Brosnihan Joe G Hollyfield |
author_sort |
Preenie deS Senanayake |
title |
Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril |
title_short |
Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril |
title_full |
Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril |
title_fullStr |
Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril |
title_full_unstemmed |
Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril |
title_sort |
retinal angiotensin ii and angiotensin-(1-7) response to hyperglycemia and an intervention with captopril |
publisher |
Hindawi - SAGE Publishing |
series |
Journal of the Renin-Angiotensin-Aldosterone System |
issn |
1752-8976 |
publishDate |
2018-08-01 |
description |
Hypothesis: Hyperglycemia decreases angiotensin-(1-7), the endogenous counter-regulator of angiotensin II in the retina. Materials and methods: The distribution and levels of retinal angiotensin II (Ang II) and angiotensin-(1-7) (Ang-(1-7)) were evaluated by confocal imaging and quantitative immunohistochemistry during the development of streptozotocin-induced diabetes in rats. Results: In the nondiabetic eye, Ang II was localized to the endfeet of Müller cells, extending into the cellular processes of the inner plexiform layer and inner nuclear layer; Ang-(1-7) showed a wider distribution, extending from the foot plates of the Müller cells to the photoreceptor layer. Eyes from diabetic animals showed a higher intensity and extent of Ang II staining compared with nondiabetic eyes, but lower intensity with a reduced distribution of Ang-(1-7) immunoreactivity. Treatment of the diabetic animals with the angiotensin-converting enzyme inhibitor (ACEI) captopril showed a reduced intensity of Ang II staining, whereas increased intensity and distribution were evident with Ang-(1-7) staining. Conclusions: These studies reveal that pharmacological inhibition with ACEIs may provide a specific intervention for the management of the diabetes-induced decline in retinal function, reversing the profile of the endogenous angiotensin peptides closer to the normal condition. |
url |
https://doi.org/10.1177/1470320318789323 |
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