ArticleJournal of the American Heart Association2014
Traumatic brain injury disrupts cerebrovascular tone through endothelial inducible nitric oxide synthase expression and nitric oxide gain of function.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
- Nitric oxide and traumatic brain injury.Medical gas research · 2027Review
- Repeated ethanol exposure in female rats impairs cerebral endothelial function and increases cerebrovascular stiffness.European journal of pharmacology · 2026Article
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
- Therapeutic Gases in Biomedicine: Updates on Nitric Oxide and Beyond.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Persistent dysmorphology and dysfunction of the brain microvasculature following repeated trauma.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression.Molecular neurodegeneration advances · 2026Article
- Delivery of a fibrin-binding hemostatic polymer ameliorates neurovascular damage and neural tissue loss after traumatic brain injury.Science advances · 2025Article
- Traumatic brain injury causes early aggregation of beta-amyloid peptides and NOTCH3 reduction in vascular smooth muscle cells of leptomeningeal arteries.Acta neuropathologica · 2025Article
- Neurological Manifestations Following Traumatic Brain Injury: Role of Behavioral, Neuroinflammation, Excitotoxicity, Nrf-2 and Nitric Oxide.CNS & neurological disorders drug targets · 2025Review
- Pathogenic soluble tau peptide disrupts endothelial calcium signaling and vasodilation in the brain microvasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Oxidative Stress and Cerebral Vascular Tone: The Role of Reactive Oxygen and Nitrogen Species.International journal of molecular sciences · 2024Review
- Systemic treatment with ubiquitin carboxy terminal hydrolase L1 TAT protein ameliorates axonal injury and reduces functional deficits after traumatic brain injury in mice.Experimental neurology · 2024Article
- Article
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
- Candidate neuroinflammatory markers of cerebral autoregulation dysfunction in human acute brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Cerebrovascular Pressure Reactivity According to Long-Pressure Reactivity Index During Spreading Depolarizations in Aneurysmal Subarachnoid Hemorrhage.Neurocritical care · 2023Article
- Interspecies and regional variability of alcohol action on large cerebral arteries: regulation by KCNMB1 proteins.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Targeting hydrogen sulfide and nitric oxide to repair cardiovascular injury after trauma.Nitric oxide : biology and chemistry · 2022Review
- Endothelial alpha globin is a nitrite reductase.Nature communications · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundTraumatic brain injury (TBI) has been reported to increase the concentration of nitric oxide (NO) in the brain and can lead to loss of cerebrovascular tone; however, the sources, amounts, and consequences of excess NO on the cerebral vasculature are unknown. Our objective was to elucidate the mechanism of decreased cerebral artery tone after TBI. METHODS AND
resultsCerebral arteries were isolated from rats 24 hours after moderate fluid‐percussion TBI. Pressure‐induced increases in vasoconstriction (myogenic tone) and smooth muscle Ca2+ were severely blunted in cerebral arteries after TBI. However, myogenic tone and smooth muscle Ca2+ were restored by inhibition of NO synthesis or endothelium removal, suggesting that TBI increased endothelial NO levels. Live native cell NO, indexed by 4,5‐diaminofluorescein (DAF‐2 DA) fluorescence, was increased in endothelium and smooth muscle of cerebral arteries after TBI. Clamped concentrations of 20 to 30 nmol/L NO were required to simulate the loss of myogenic tone and increased (DAF‐2T) fluorescence observed following TBI. In comparison, basal NO in control arteries was estimated as 0.4 nmol/L. Consistent with TBI causing enhanced NO‐mediated vasodilation, inhibitors of guanylyl cyclase, protein kinase G, and large‐conductance Ca2+‐activated potassium (BK) channel restored function of arteries from animals with TBI. Expression of the inducible isoform of NO synthase was upregulated in cerebral arteries isolated from animals with TBI, and the inducible isoform of NO synthase inhibitor 1400W restored myogenic responses following TBI.
conclusionsThe mechanism of profound cerebral artery vasodilation after TBI is a gain of function in vascular NO production by 60‐fold over controls, resulting from upregulation of the inducible isoform of NO synthase in the endothelium.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.