Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca2+-activated K+ (BK) channels. - Test2 - elhamkhani - TriplyDB

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca2+-activated K+ (BK) channels.

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca2+-activated K+ (BK) channels.

http://www.wikidata.org/entity/Q30514232

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The vascular conducted response in cerebral blood flow regulation Vascular inward rectifier K+ channels as external K+ sensors in the control of cerebral blood flow Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature BK Channels in the Central Nervous System.Stress-induced glucocorticoid signaling remodels neurovascular coupling through impairment of cerebrovascular inwardly rectifying K+ channel function CO2 has no therapeutic effect on early microvasospasm after experimental subarachnoid hemorrhage Pituitary adenylate cyclase activating polypeptide (PACAP) dilates cerebellar arteries through activation of large-conductance Ca(2+)-activated (BK) and ATP-sensitive (K ATP) K (+) channels.Higher brain extracellular potassium is associated with brain metabolic distress and poor outcome after aneurysmal subarachnoid hemorrhage.Regulation of neurovascular coupling in autoimmunity to water and ion channels Impact of heme and heme degradation products on vascular diameter in mouse visual cortex Dysfunction of mouse cerebral arteries during early aging.SAH-induced MMP activation and K V current suppression is mediated via both ROS-dependent and ROS-independent mechanisms.A role of the sodium pump in spreading ischemia in rats.Retinal Vessel Analysis (RVA) in the Context of Subarachnoid Hemorrhage - A Proof of Concept Study.Requisite ischemia for spreading depolarization occurrence after subarachnoid hemorrhage in rodents.Astrocyte Ca2+ Signaling Drives Inversion of Neurovascular Coupling after Subarachnoid Hemorrhage BK Channels in Cardiovascular Diseases and Aging Astrocyte-induced cortical vasodilation is mediated by D-serine and endothelial nitric oxide synthase.Ion channel networks in the control of cerebral blood flow.Subarachnoid hemorrhage, spreading depolarizations and impaired neurovascular coupling.Ryanodine receptors, calcium signaling, and regulation of vascular tone in the cerebral parenchymal microcirculation.Prostaglandin E2, a postulated astrocyte-derived neurovascular coupling agent, constricts rather than dilates parenchymal arterioles.Microvascular Dysfunction and Cognitive Impairment.The role of the microcirculation in delayed cerebral ischemia and chronic degenerative changes after subarachnoid hemorrhage.Proposed toxic and hypoxic impairment of a brainstem locus in autism.Neurovascular signaling in the brain and the pathological consequences of hypertension.Controversies and evolving new mechanisms in subarachnoid hemorrhage.Delayed neurological deterioration after subarachnoid haemorrhage.Plasticity of cerebrovascular smooth muscle cells after subarachnoid hemorrhage.Subarachnoid hemorrhage: a review of experimental studies on the microcirculation and the neurovascular unit.Spreading depolarization in the ischemic brain: does aging have an impact?TRPC Channels and Stroke.Binaural blood flow control by astrocytes: listening to synapses and the vasculature.Astrocyte dysfunction in Alzheimer disease.Activation of TRPV4 channels does not mediate inversion of neurovascular coupling after SAH.Purinergic signaling triggers endfoot high-amplitude Ca2+ signals and causes inversion of neurovascular coupling after subarachnoid hemorrhage.The yin and yang of KV channels in cerebral small vessel pathologies.Turing-like structures in a functional model of cortical spreading depression.Inhibition of vascular smooth muscle inward-rectifier K+ channels restores myogenic tone in mouse urinary bladder arterioles.Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo.

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P2860

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca2+-activated K+ (BK) channels.

http://www.wikidata.org/entity/Q30514232

description

2012 nî lūn-bûn

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2012 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2012 թվականի ապրիլին հրատարակված գիտական հոդված

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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name

Inversion of neurovascular cou ...... 2+-activated K+ (BK) channels.

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Inversion of neurovascular cou ...... 2+-activated K+ (BK) channels.

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Inversion of neurovascular cou ...... 2+-activated K+ (BK) channels.

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Inversion of neurovascular cou ...... 2+-activated K+ (BK) channels.

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Inversion of neurovascular cou ...... 2+-activated K+ (BK) channels.

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Inversion of neurovascular cou ...... 2+-activated K+ (BK) channels.

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Inversion of neurovascular cou ...... a2+-activated K+ (BK) channels

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Adrian D Bonev

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George C Wellman

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Masayo Koide

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P2860

Cerebral vasospasm after subarachnoid hemorrhage: the emerging revolution

Compartmentalized beta subunit distribution determines characteristics and ethanol sensitivity of somatic, dendritic, and terminal large-conductance calcium-activated potassium channels in the rat central nervous system

Neurovascular regulation in the normal brain and in Alzheimer's disease

Glial and neuronal control of brain blood flow

Glial cells dilate and constrict blood vessels: a mechanism of neurovascular coupling

Astrocytic endfoot Ca2+ and BK channels determine both arteriolar dilation and constriction.

Limitations of collateral flow after occlusion of a single cortical penetrating arteriole

Reduced Ca2+ spark activity after subarachnoid hemorrhage disables BK channel control of cerebral artery tone.

Tone-dependent vascular responses to astrocyte-derived signals.

Estimating intracellular calcium concentrations and buffering without wavelength ratioing.

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