Retinal arteriolar responses to acute severe elevation in systemic blood pressure in cats: Role of endothelium-derived factors

Nakabayashi, Seigo; Nagaoka, Taiji; Tani, Tomofumi; Sogawa, Kenji; Hein, Travis W.; Li, Kuo; Yoshida, Akitoshi

doi:10.1016/j.exer.2012.08.007

Cited by 18 publications

(14 citation statements)

References 30 publications

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“…Our model predicts that a sudden increase in arterial pressure leads to an increase in blood flow and, consequently, an increase in the O 2 levels within the vessels and inside the retinal tissue. These results are consistent with the experimental observations in cats (Nakabayashi et al 2012), where acute severe elevation in systemic blood pressure resulted in sudden increases in blood velocity and retinal blood flow. Changes in plasma viscosity (μ p ) Plasma viscosity has a strong influence on the O 2 tension at the level of the retinal ganglion cells, p t -RGC.…”

Section: Simulation Results In Baseline Conditionssupporting

confidence: 94%

Blood flow mechanics and oxygen transport and delivery in the retinal microcirculation: multiscale mathematical modeling and numerical simulation

Causin

Guidoboni

Malgaroli

et al. 2015

Biomech Model Mechanobiol

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Section: Simulation Results In Baseline Conditionssupporting

confidence: 94%

Blood flow mechanics and oxygen transport and delivery in the retinal microcirculation: multiscale mathematical modeling and numerical simulation

Causin

Guidoboni

Malgaroli

et al. 2015

Biomech Model Mechanobiol

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“…The American Journal of Pathology -ajp.amjpathol.org 3041 injection of BQ-123 (30 mg/50 mL per eye, 1 mmol/L) or BQ-788 (33 mg/50 mL per eye, 1 mmol/L) injected into the vitreous was sufficient to elicit a maximum retinal hemodynamic response. 23,24 We tested several concentrations of both receptor blockers (BQ-123: 10, 17, and 34 mg/mL per eye; BQ-788: 1.5, 4.5, and 13.5 mg/mL per eye) to find the appropriate concentrations that would ensure maximum response. We determined that 17 mg/mL per eye of BQ-123 (28 mmol/L) and 4.5 mg/mL per eye of BQ-788 (6.8 mmol/L) were optimal for our studies.…”

Section: Treatment Of Animalsmentioning

confidence: 99%

Activation of the Endothelin System Mediates Pathological Angiogenesis during Ischemic Retinopathy

Patel

Narayanan

Zhang

et al. 2014

The American Journal of Pathology

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Retinopathy of prematurity adversely affects premature infants because of oxygen-induced damage of the immature retinal vasculature, resulting in pathological neovascularization (NV). Our pilot studies using the mouse model of oxygen-induced retinopathy (OIR) showed marked increases in angiogenic mediators, including endothelins and endothelin receptor (EDNR) A. We hypothesized that activation of the endothelin system via EDNRA plays a causal role in pathological angiogenesis and up-regulation of angiogenic mediators, including vascular endothelial growth factor A (VEGFA) in OIR. Mice were exposed to 75% oxygen from post-natal day P7 to P12, treated with either vehicle or EDNRA antagonist BQ-123 or EDNRB antagonist BQ-788 on P12, and kept at room air from P12 to P17 (ischemic phase). RT-PCR analysis revealed increased levels of EDN2 and EDNRA mRNA, and Western blot analysis revealed increased EDN2 expression during the ischemic phase. EDNRA inhibition significantly increased vessel sprouting, resulting in enhanced physiological angiogenesis and decreased pathological NV, whereas EDNRB inhibition modestly improved vascular repair. OIR triggered significant increases in VEGFA protein and mRNA for delta-like ligand 4, apelin, angiopoietin-2, and monocyte chemoattractant protein-1. BQ-123 treatment significantly reduced these alterations. EDN2 expression was localized to retinal glia and pathological NV tufts of the OIR retinas. EDN2 also induced VEGFA protein expression in cultured astrocytes. In conclusion, inhibition of the EDNRA during OIR suppresses pathological NV and promotes physiological angiogenesis.

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“…The discrepancy between these previous studies may reflect the effect of increased systemic BP before flicker stimuli. Because we recently reported that acutely elevated systemic BP leads to increased RBF due to release of NO and prostanoids probably through a shear stress-induced vasodilation mechanism in cats, 10 it is unclear how NO contributes to flicker-induced retinal hyperemia.…”

Section: R Etinal Vessels Dilate and Retinal Blood Flow (Rbf) Increasesmentioning

confidence: 99%

Role of Neuronal Nitric Oxide Synthase in Regulating Retinal Blood Flow During Flicker-Induced Hyperemia in Cats

Yoshioka

Nagaoka

Song

et al. 2015

Invest. Ophthalmol. Vis. Sci.

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Retinal arteriolar responses to acute severe elevation in systemic blood pressure in cats: Role of endothelium-derived factors

Cited by 18 publications

References 30 publications

Blood flow mechanics and oxygen transport and delivery in the retinal microcirculation: multiscale mathematical modeling and numerical simulation

Blood flow mechanics and oxygen transport and delivery in the retinal microcirculation: multiscale mathematical modeling and numerical simulation

Activation of the Endothelin System Mediates Pathological Angiogenesis during Ischemic Retinopathy

Role of Neuronal Nitric Oxide Synthase in Regulating Retinal Blood Flow During Flicker-Induced Hyperemia in Cats

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