scholarly journals A mathematical model for the role of N 2 O 3 in enhancing nitric oxide bioavailability following nitrite infusion

Nitric Oxide ◽  
2016 ◽  
Vol 60 ◽  
pp. 1-9 ◽  
Author(s):  
Yien Liu ◽  
Donald G. Buerk ◽  
Kenneth A. Barbee ◽  
Dov Jaron
Keyword(s):  
Nitric Oxide ◽  
Mathematical Model ◽  
Nitric Oxide Bioavailability

Tracking the role of trans-ligands in ruthenium–NO bond lability: computational insight

2020 ◽  
Vol 44 (27) ◽  
pp. 11448-11456
Author(s):  
Renato Pereira Orenha ◽  
Graziele Cappato Guerra Silva ◽  
Ana Paula de Lima Batista ◽  
Antonio Gustavo Sampaio de Oliveira Filho ◽  
Nelson Henrique Morgon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bond Stability ◽  
Nitric Oxide Bioavailability

Ruthenium–NO tetraamine structures control the nitric oxide bioavailability. The ligand trans to NO modulates the Ru–NO bond stability.

scholarly journals Multiscale modeling and simulation of neurovascular coupling in the retina

2018 ◽  
Vol 2 (2) ◽  
pp. 30-35
Author(s):  
Riccardo Sacco ◽  
Aurelio G. Mauri ◽  
Alessandra Cardani ◽  
Brent A. Siesky ◽  
Giovanna Guidoboni ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mathematical Model ◽  
Diabetic Retinopathy ◽  
Multiscale Modeling ◽  
Neurovascular Coupling ◽  
Retinal Arterioles ◽  
Potent Vasodilator ◽  
Simulation Results ◽  
Flicker Light

The role of nitric oxide (NO), usually considered as a potent vasodilator, in regulating retinal neurovascular coupling is still elusive. Measurements of flicker light-induced functional hyperemia (FH) in humans show that an increase of NO levels reduces vasodilation. This evidence has led to conjecture that such an increase may be responsible for suppressing flicker-evoked vasodilation in diabetic retinopathy. In this paper, we propose a mathematical model to theoretically investigate the effect of an increase in neural NO (nNO) on the vasodilation of retinal arterioles. Simulation results indicate that nNO increase may:1. significantly aff ect vasoconstrictive agent production by glial cells; and2. elicit vasoconstriction rather than vasodilation in retinal arterioles.Model predictions seem therefore to support the conjecture that NO increase may be responsible for suppressing flicker-evoked vasodilation in diabetic retinopathy.

Procyanidins extracted from the litchi pericarp ameliorate atherosclerosis in ApoE knockout mice: their effects on nitric oxide bioavailability and oxidative stress

2017 ◽  
Vol 8 (11) ◽  
pp. 4210-4216 ◽  
Author(s):  
Shuang Rong ◽  
Xueting Hu ◽  
Siqi Zhao ◽  
Yanting Zhao ◽  
Xiao Xiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiovascular Diseases ◽  
Knockout Mice ◽  
Epidemiological Studies ◽  
Apoe Knockout Mice ◽  
And Oxidative Stress ◽  
Litchi Pericarp ◽  
Nitric Oxide Bioavailability

Epidemiological studies strongly support the role of procyanidin-rich beverages and fruit in the prevention of cardiovascular diseases.

scholarly journals Exercise training and muscle microvascular oxygenation: role of nitric oxide bioavailability

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Daniel M Hirai ◽  
Steven W Copp ◽  
Scott K Ferguson ◽  
Clark T Holdsworth ◽  
Timothy I Musch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Exercise Training ◽  
Microvascular Oxygenation ◽  
Nitric Oxide Bioavailability

scholarly journals Role of nitric oxide in the regulation of digital pulse volume amplitude in humans

2006 ◽  
Vol 101 (2) ◽  
pp. 545-548 ◽  
Author(s):  
Anju Nohria ◽  
Marie Gerhard-Herman ◽  
Mark A. Creager ◽  
Shauna Hurley ◽  
Debi Mitra ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Healthy Subjects ◽  
Reactive Hyperemia ◽  
Nitric Oxide Synthesis ◽  
Pulse Volume ◽  
Digital Pulse ◽  
Peripheral Arterial ◽  
Nitric Oxide Bioavailability

Measurement of the increase in digital pulse volume amplitude (PVA) during reactive hyperemia relative to baseline (PVA-RH) is being applied widely as a convenient test of nitric oxide bioavailability. However, evidence linking digital PVA-RH to nitric oxide is currently lacking. Accordingly, we investigated whether nitric oxide is responsible for the increase in digital PVA. During reactive hyperemia, we used a peripheral arterial tonometer to record digital PVA at baseline and during reactive hyperemia. The role of nitric oxide in these responses was investigated in 19 healthy subjects by inhibiting nitric oxide synthesis with NG-nitro-l-arginine methyl ester (l-NAME). Ten subjects underwent the identical protocol with saline and five with phenylephrine, a nonspecific vasoconstrictor, instead of l-NAME. The change in digital PVA after drug administration was compared between the three groups. Relative to the response with saline (−5 ± 2%), baseline PVA was unchanged by l-NAME infusion (−10 ± 2%), but it decreased significantly with phenylephrine (−50 ± 12%; P = 0.003). PVA-RH increased slightly with saline infusion (9 ± 4%). In comparison, PVA-RH was significantly blunted by l-NAME administration (−46 ± 21%; P = 0.002) and was relatively unchanged by phenylephrine (20 ± 9%). The present study establishes a central role for nitric oxide in the augmentation of PVA during reactive hyperemia. The measurement of digital PVA-RH may indeed provide a simple means of assessing endothelial function in humans.

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