Uncoupling of eNOS causes superoxide anion production and impairs NO signaling in the cerebral microvessels of hph-1 mice.
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Cerebral Small Vessel Disease: Targeting Oxidative Stress as a Novel Therapeutic Strategy?Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitusTetrahydrobiopterin activates brown adipose tissue and regulates systemic energy metabolism.Erythropoietin increases bioavailability of tetrahydrobiopterin and protects cerebral microvasculature against oxidative stress induced by eNOS uncouplingErythropoietin prevents endothelial dysfunction in GTP-cyclohydrolase I-deficient hph1 miceP2X(7) receptor in the kidneys of diabetic rats submitted to aerobic training or to N-acetylcysteine supplementation [corrected].Overexpression of mitochondrial antioxidant manganese superoxide dismutase (MnSOD) provides protection against AZT- or 3TC-induced endothelial dysfunction.Regional Heterogeneity of Cerebral Microvessels and Brain Susceptibility to Oxidative StressCharacterization of cerebral microvasculature in transgenic mice with endothelium targeted over-expression of GTP-cyclohydrolase I.PPARδ agonist GW501516 prevents uncoupling of endothelial nitric oxide synthase in cerebral microvessels of hph-1 mice.Effects of angiotensin II on the cerebral circulation: role of oxidative stress.Genetic elimination of eNOS reduces secondary complications of experimental subarachnoid hemorrhage.Expression and Processing of Amyloid Precursor Protein in Vascular Endothelium.Age-Related Modulations of AQP4 and Caveolin-1 in the Hippocampus Predispose the Toxic Effect of Phoneutria nigriventer Spider Venom.Acute tetrahydrobiopterin supplementation attenuates sympathetic vasoconstrictor responsiveness in resting and contracting skeletal muscle of healthy rats.Uncoupling of endothelial nitric oxide synthase in cerebral vasculature of Tg2576 mice.Endothelium-specific amyloid precursor protein deficiency causes endothelial dysfunction in cerebral arteries.Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction.Endothelial microparticles increase in mitral valve disease and impair mitral valve endothelial function.Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia-Ischemia
P2860
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P2860
Uncoupling of eNOS causes superoxide anion production and impairs NO signaling in the cerebral microvessels of hph-1 mice.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
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2012年论文
@zh-cn
name
Uncoupling of eNOS causes supe ...... al microvessels of hph-1 mice.
@ast
Uncoupling of eNOS causes supe ...... al microvessels of hph-1 mice.
@en
type
label
Uncoupling of eNOS causes supe ...... al microvessels of hph-1 mice.
@ast
Uncoupling of eNOS causes supe ...... al microvessels of hph-1 mice.
@en
prefLabel
Uncoupling of eNOS causes supe ...... al microvessels of hph-1 mice.
@ast
Uncoupling of eNOS causes supe ...... al microvessels of hph-1 mice.
@en
P2093
P2860
P1476
Uncoupling of eNOS causes supe ...... al microvessels of hph-1 mice.
@en
P2093
Anantha Vijay R Santhanam
Leslie A Smith
Livius V d'Uscio
Zvonimir S Katusic
P2860
P304
P356
10.1111/J.1471-4159.2012.07872.X
P407
P577
2012-08-03T00:00:00Z