Retinal angiotensin II and angiotensin-(1-7) response to hyperglycemia and an
intervention with captopril.
Authors Senanayake PD, Bonilha VL, W Peterson J, Yamada Y, Karnik SS, Daneshgari F,
Brosnihan KB, Hollyfield JG
Submitted By Firouz Daneshgari on 9/4/2018
Status Published
Journal Journal of the renin-angiotensin-aldosterone system : JRAAS
Year 2018
Date Published
Volume : Pages 19 : Not Specified
PubMed Reference 30126320
Abstract Hyperglycemia decreases angiotensin-(1-7), the endogenous counter-regulator of
angiotensin II in the retina., 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., 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., 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.

Investigators with authorship
Firouz DaneshgariCase Western Reserve