ArticleStroke2008
Oxyhemoglobin-induced expression of R-type Ca2+ channels in cerebral arteries.
Article in Stroke, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Bio-inspired spatiotemporal cascade reaction liposome for ferroptosis treatment following subarachnoid hemorrhage.Materials today. Bio · 2026Article
- The L-type calcium channel CaV1.3: A potential target for cancer therapy.Journal of cellular and molecular medicine · 2024Review
- Oxidative Stress and Intracranial Hypertension after Aneurysmal Subarachnoid Hemorrhage.Antioxidants (Basel, Switzerland) · 2022Review
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Andrographolide Attenuates Blood-Brain Barrier Disruption, Neuronal Apoptosis, and Oxidative Stress Through Activation of Nrf2/HO-1 Signaling Pathway in Subarachnoid Hemorrhage.Neurotoxicity research · 2022Article
- Concentrations of estradiol, progesterone and testosterone in sefrum and cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage correlate weakly with transcranial Doppler flow velocities.BMC neuroscience · 2021Article
- Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage.Frontiers in cellular neuroscience · 2021Review
- Haptoglobin administration into the subarachnoid space prevents hemoglobin-induced cerebral vasospasm.The Journal of clinical investigation · 2019Article
- An introduction to the pathophysiology of aneurysmal subarachnoid hemorrhage.Neurosurgical review · 2018Review
- Unconjugated bilirubin modulates neuronal signaling only in wild-type mice, but not after ablation of the R-type/CaCNS neuroscience & therapeutics · 2018Article
- The yin and yang of KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- PPARβ/δ, a Novel Regulator for Vascular Smooth Muscle Cells Phenotypic Modulation and Vascular Remodeling after Subarachnoid Hemorrhage in Rats.Scientific reports · 2017Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- R-Type CaExperimental physiology · 2017Article
- Astrocyte Ca2+ Signaling Drives Inversion of Neurovascular Coupling after Subarachnoid Hemorrhage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Hypoxia-dependent reactive oxygen species signaling in the pulmonary circulation: focus on ion channels.Antioxidants & redox signaling · 2015Review
- Case report: Intra-procedural aneurysm rupture during endovascular treatment causing immediate, transient angiographic vasospasm.Journal of vascular and interventional neurology · 2014Article
- Therapeutic implications of estrogen for cerebral vasospasm and delayed cerebral ischemia induced by aneurysmal subarachnoid hemorrhage.BioMed research international · 2014Review
- Sulforaphane enhances the activity of the Nrf2-ARE pathway and attenuates inflammation in OxyHb-induced rat vascular smooth muscle cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
- The changing landscape of voltage-gated calcium channels in neurovascular disorders and in neurodegenerative diseases.Current neuropharmacology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeCerebral vasospasm after subarachnoid hemorrhage (SAH) is a major contributor to mortality and morbidity after aneurysm rupture. Recently, R-type voltage-dependent Ca(2+) channel (VDCC) expression has been associated with increased cerebral artery constriction in a rabbit model of SAH. The goal of the present study was to examine whether the blood component oxyhemoglobin (oxyHb) can mimic the ability of SAH to cause R-type VDCC expression in the cerebral vasculature.
methodsRabbit cerebral arteries were organ cultured in serum-free media for up to 5 days in the presence or absence of purified oxyHb (10 micromol/L). Diameter changes in response to diltiazem, (L-type VDCC antagonist) and SNX-482 (R-type VDCC antagonist) were recorded at day 1, 3, or 5 in arteries constricted by elevated extracellular potassium. RT-PCR was performed on RNA extracted from arteries cultured for 5 days (+/-oxyHb) to assess VDCC expression.
resultsAfter 5 days, oxyHb-treated arteries were less sensitive and partially resistant to diltiazem compared to similar arteries organ cultured in the absence of oxyHb. Further, SNX-482 dilated arteries organ cultured for 5 days in the presence, but not in the absence, of oxyHb. RT-PCR revealed that oxyHb treated arteries expressed R-type VDCCs (Ca(V) 2.3) in addition to L-type VDCCs (Ca(V) 1.2), whereas untreated arteries expressed only Ca(V) 1.2.
conclusionsThese results demonstrate that oxyhemoglobin exposure for 5 days induces the expression of Ca(V) 2.3 in cerebral arteries. We propose that oxyhemoglobin contributes to enhanced cerebral artery constriction after SAH via the emergence of R-type VDCCs.
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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.