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Control of microvascular function by ion channels

Control of microvascular function by ion channels
离子通道控制微血管功能
批准号:
10201230
负责人:
Adebowale Adebiyi
金额:
$2.34万
依托单位国家:
美国
项目类别:
财政年份:
2020
资助国家:
美国
项目状态:
已结题
起止时间:
2020-12-22 至 2024-03-31
关键词:
AblationAcuteAddressAdrenergic AgentsAnionsBiological MarkersBlood PressureBlood VesselsBlood VolumeCardiovascular DiseasesCatecholaminesCationsCellsChronicCisplatinDataDiseaseElectrolytesEndothelial CellsEndotheliumExocytosisExperimental ModelsFunctional disorderGenerationsGlomerular Filtration RateHistologyHypertensionImaging TechniquesImpairmentIn VitroInjury to KidneyIon ChannelKidneyKidney DiseasesKidney FailureKnowledgeLasersLifeLiteratureMediatingMembrane ProteinsMesenteryMicrocirculationMicroscopyModelingMusMyocardial InfarctionNerveNerve EndingsNeuronsNeurotransmitter ReceptorNorepinephrineOrganOxidantsOxidation-ReductionOxidative StressPC12 CellsPathway interactionsPerfusionPeripheralPermeabilityPharmacologyPhenotypePhysiologicalPhysiologyPilot ProjectsPlasmaPreventionPublic HealthPublishingReactive Oxygen SpeciesRegional Blood FlowRenal functionRoleSensorySensory ReceptorsSignal PathwaySignal TransductionSmooth MuscleSmooth Muscle MyocytesStressStrokeSympathectomySystemTechniquesTelemetryTestingTimeUnited StatesVascular DiseasesVascular Smooth MuscleVascular resistanceVenousafferent nervealpha-adrenergic receptordecubitus ulcerextracellulargenetic approachhemodynamicshypoperfusionimaging approachin vivoinsightkidney dysfunctionmimeticsmultiphoton microscopyneurotransmissionneurotransmitter releasenovelpostsynapticpressurepresynaptic neuronsreceptorrelating to nervous systemrenal damageresponsestemtherapeutic targetultrasound microscopyvascular bedvascular injuryvasoconstriction

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中文摘要
翻译
血管平滑肌细胞连接后神经递质受体的激活调节血管张力
英文摘要
Activation of post-junctional neurotransmitter receptors in vascular smooth muscle cells modulates vascular tone and causes significant alterations in organ perfusion, mechanisms of which may be amplified or reduced in cardiovascular and renal disease. Neurotransmitter release from presynaptic nerve terminals is highly dependent on extracellular Ca2+ influx. Thus, modulation of Ca2+-permeable channels in neurons that impinge on microvessels can alter microcirculation by regulating neurotransmission. A large body of literature has elucidated the role of vascular smooth muscle and endothelial cell Ca2+ signaling in the control of microvascular function. However, there remains a significant knowledge gap on the function and pathophysiology of perivascular nerve ion channels in microcirculation. The current application stems from pilot studies that uncovered a new role for the transient receptor potential melastatin 8 (TRPM8) channels outside of sensory signaling. We propose an intriguing concept that a subset of peripheral sympathetic nerves (sn) expresses TRPM8 channels. Our data suggest that snTRPM8 is redox-sensitive and that the responses mediated by perivascular snTRPM8 channels alter vascular resistance via smooth muscle cell adrenergic system. We will use a repertoire of physiological; pharmacological; and high- content imaging approaches to study the central hypothesis that snTRPM8 activation increases vascular resistance and reduces vascular bed perfusion via Ca2+-dependent catecholamine neurotransmission and that this pathway contributes to oxidative stress-induced vascular dysfunction. To address this hypothesis, three specific aims will be investigated. Aim 1 will test the hypothesis that perivascular snTRPM8 activation reduces microcirculation via sn-dependent vasoconstriction. Aim 2 will study the hypothesis that redox-evoked snTRPM8 channel activation increases vascular resistance. Aim 3 will explore the concept that snTRPM8-dependent sympathoexcitation contributes to oxyradical-induced vascular dysfunction and renal damage. This project will utilize selective pharmacological modulators of TRPM8 channels and mice with global and sn-specific TRPM8 deletion. Techniques to investigate microcirculation include transit-time ultrasound, laser-Doppler, and multiphoton microscopy.
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Urotensin II and renal insufficiency in growth-restricted infants.
Control of microvascular function by ion channels
Control of microvascular function by ion channels
Control of microvascular function by ion channels
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