2024
N-Methyl-D-aspartic acid (NMDA) mediated vasodilation in aorta
Yilmaz G, Alexander J. N-Methyl-D-aspartic acid (NMDA) mediated vasodilation in aorta. Physiology 2024, 39: 2323. DOI: 10.1152/physiol.2024.39.s1.2323.Peer-Reviewed Original ResearchN-methyl-D-aspartic acidNitric oxide synthaseVascular smooth muscleVascular responsesSmooth muscleN-methyl-D-aspartic acid receptor blockadeResponse to NMDAWild type male miceNMDA-induced vasodilationNon-NMDA receptorsIn vitro myographyThoracic aorta segmentsPeripheral vascular responseMK-801Receptor blockadeNMDA concentrationsNMDA receptorsResistance arteriesEndothelial cell layerL-NAMEOsmolarity solutionVasodilatory effectMethyl ester hydrochlorideAortic segmentsInduce vasodilation
2022
L-ARGININE PREVENTS ISCHEMIC INJURY IN EXPLANTED RAT INTESTINAL REGIONS IN AN EX VIVO PERFUSION MODEL
Finotti M, Barahona M, Maina R, Lysyy T, Agarwal R, Schmitt P, Caturegli G, Di Renzo C, Anselmo A, Mulligan D, Geibel J, D'Amico F. L-ARGININE PREVENTS ISCHEMIC INJURY IN EXPLANTED RAT INTESTINAL REGIONS IN AN EX VIVO PERFUSION MODEL. Transplantation Reports 2022, 7: 100096. DOI: 10.1016/j.tpr.2022.100096.Peer-Reviewed Original ResearchIschemic injuryIntestinal segmentsIschemic damageIntraluminal perfusionNitric oxide-arginine pathwayMale Sprague-Dawley ratsN-nitroarginine methyl esterSprague-Dawley ratsEx vivo perfusion modelVivo perfusion modelNon-ischemic conditionsSmall intestinal segmentsFITC-inulinExtraluminal sideL-NAMEReperfusion injuryProtective effectL-arginineSmall intestinePerfusion modelInjuryIntestinal regionsFluid secretionReduced susceptibilityPerfusion
2020
Penicillin G Induces H+, K+-ATPase via a Nitric Oxide-Dependent Mechanism in the Rat Colonic Crypt
Baratta VM, Norz V, Barahona MJ, Gisinger TM, Mulligan D, Geibel JP. Penicillin G Induces H+, K+-ATPase via a Nitric Oxide-Dependent Mechanism in the Rat Colonic Crypt. Cellular Physiology And Biochemistry 2020, 54: 1132-1142. PMID: 33175479, PMCID: PMC8095381, DOI: 10.33594/000000305.Peer-Reviewed Original ResearchConceptsRat colonic cryptsColonic cryptsNitric oxideNitric oxide-dependent mechanismPotassium homeostasisArginine methyl esterAmmonium prepulse techniqueIntracellular nitric oxideSodium-free conditionsL-NAMEDiarrheal statesATPase activityBACKGROUND/Presence of NOPenicillin G sodium saltAcute exposureL-arginineSmall intestineIsolated administrationN-nitroHomeostatic conditionsCryptsPrepulse techniqueSignificant reductionNovel mechanism
2019
Induction of Secretagogue Independent Gastric Acid Secretion via a Novel Aspirin-Activated Pathway
Kitay AM, Ferstl FS, Link A, Geibel JP. Induction of Secretagogue Independent Gastric Acid Secretion via a Novel Aspirin-Activated Pathway. Frontiers In Physiology 2019, 10: 1264. PMID: 31649553, PMCID: PMC6795678, DOI: 10.3389/fphys.2019.01264.Peer-Reviewed Original ResearchGastric acid secretionNon-selective NOS inhibitor L-NAMENOS inhibitor L-NAMEInhibitor L-NAMEAcid secretionL-NAMESoluble guanylyl cyclase inhibitor 1HGuanylyl cyclase inhibitor 1HIncreases nitric oxide productionUsage of aspirinGastric glandsPH-sensitive dye BCECF-AMNitric oxide productionVariety of cancersNovel secretagogueBlood clot formationAspirin exposureChronic conditionsMucosal barrierRepetitive dosesUlcer formationAspirin consumptionBasolateral exposureAspirinClot formation
2018
Prevention of Ischemic Injury in Colon and Small Intestine in an Ex Vivo Perfusion Animal Model
Finotti M, Lysyy T, Barahona M, Maina R, Caturegli G, D'Amico F, Mulligan D, Geibel J. Prevention of Ischemic Injury in Colon and Small Intestine in an Ex Vivo Perfusion Animal Model. Transplantation 2018, 102: s709. DOI: 10.1097/01.tp.0000543675.85457.d2.Peer-Reviewed Original ResearchIschemia-reperfusion injuryIschemic injuryIschemic damageL-arginineSmall intestineL-NAMEDistal colonPerfusion machineMale Sprague-Dawley ratsIntestinal ischemic damageIntestinal ischemic injuryAnti-ischemic effectsSprague-Dawley ratsIntestinal graftInflammatory injuryInflammatory pathwaysIntestinal viabilityProtective effectAbdominal cavityColon segmentsIschemic conditionsIntestinal wallIntraluminal secretionsAnimal modelsIntestine segments
2017
Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats
Kitay AM, Link A, Geibel JP. Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats. Cellular Physiology And Biochemistry 2017, 44: 1606-1615. PMID: 29212068, DOI: 10.1159/000485755.Peer-Reviewed Original ResearchConceptsNitric oxide synthaseGastric acid secretionAcid secretionL-arginineL-NAMENO/sGC/cGMP pathwayNitric oxideSGC/cGMP pathwayParietal cellsNitric oxide synthase stimulationSGC inhibitor ODQL-arginine exposureAcid-related diseasesPossible intracellular mechanismsNovel secretagogueRat parietal cellsIsolated gastric glandsUlcer diseaseOxide synthaseCGMP pathwayImmune functionImportant mediatorIntracellular mechanismsSecretionGastric glandsL-theanine prevent quinolinic acid induced motor deficit and striatal neurotoxicity: Reduction in oxido-nitrosative stress and restoration of striatal neurotransmitters level
Jamwal S, Singh S, Gill JS, Kumar P. L-theanine prevent quinolinic acid induced motor deficit and striatal neurotoxicity: Reduction in oxido-nitrosative stress and restoration of striatal neurotransmitters level. European Journal Of Pharmacology 2017, 811: 171-179. PMID: 28624333, DOI: 10.1016/j.ejphar.2017.06.016.Peer-Reviewed Original ResearchConceptsStriatal neurotransmitter levelsOxido-nitrosative stressNeurotransmitter levelsProtective effectL-NAMEMotor deficitsQuinolinic acidL-arginineL-theanineNitric oxide synthase inhibitorPro-inflammatory cytokinesNitric oxide pathwayOxide synthase inhibitorOpen field testL-theanine treatmentRota-rodBeam walkingNeuro-inflammationNeurotransmitter alterationsNeuroprotective potentialStriatal neurotoxicityOxide pathwayQA injectionGrip strengthMotor coordination
2016
L-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway
Jamwal S, Kumar P. L-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway. Molecular Neurobiology 2016, 54: 2327-2337. PMID: 26957301, DOI: 10.1007/s12035-016-9822-5.Peer-Reviewed Original ResearchConceptsHuntington's diseaseStriatal toxicityL-NAMENeuroprotective potentialConcurrent treatmentProtective effectBody weightL-arginineL-theanineGABAergic medium spiny neuronsGreen tea preventsStriatal neurotransmitter levelsPro-inflammatory mediatorsPro-inflammatory cytokinesNitric oxide pathwayBlood-brain barrierMedium spiny neuronsNitric oxide productionL-theanine treatmentNeurotransmitter alterationsOxide pathwayBrain barrierSpiny neuronsNeurotransmitter levelsRat striatum
2012
Protection against L‐NAME‐induced reduction in cardiac output persists even after cessation of angiotensin‐converting enzyme inhibitor treatment
Biwer L, Broderick T, Xu H, Carroll C, Hale T. Protection against L‐NAME‐induced reduction in cardiac output persists even after cessation of angiotensin‐converting enzyme inhibitor treatment. Acta Physiologica 2012, 207: 156-165. PMID: 22834875, DOI: 10.1111/j.1748-1716.2012.02474.x.Peer-Reviewed Original ResearchConceptsL-NAMEMyocardial injuryCardiac functionEnalapril treatmentACE inhibitionCardiac outputL ratsL-NAME-induced reductionNitric oxide synthase inhibitorShort-term angiotensinTransient ACE inhibitionEnzyme inhibitor treatmentHeart failure treatmentCessation of treatmentOxide synthase inhibitorArginine methyl esterEosin-stained sectionsArterial pressureHypertensive ratsCardiac changesCardiac dysfunctionWashout periodCoronary flowMyocardial infarctionFailure treatment
2010
Hypersensitivity to Thromboxane Receptor Mediated Cerebral Vasomotion and CBF Oscillations during Acute NO-Deficiency in Rats
Horváth B, Lenzsér G, Benyó B, Németh T, Benkő R, Iring A, Hermán P, Komjáti K, Lacza Z, Sándor P, Benyó Z. Hypersensitivity to Thromboxane Receptor Mediated Cerebral Vasomotion and CBF Oscillations during Acute NO-Deficiency in Rats. PLOS ONE 2010, 5: e14477. PMID: 21217826, PMCID: PMC3013104, DOI: 10.1371/journal.pone.0014477.Peer-Reviewed Original ResearchMeSH Keywords15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidAnimalsBrainCerebrovascular CirculationEnzyme InhibitorsHypersensitivityLaser-Doppler FlowmetryMaleMiddle Cerebral ArteryMotionNG-Nitroarginine Methyl EsterNitric OxideRatsRats, WistarReceptors, Thromboxanerho-Associated KinasesSignal TransductionThromboxane A2ConceptsCerebral blood flowCBF oscillationsNitric oxideCerebral vasomotionThromboxane receptorNitro-L-arginine methyl esterDecreased cerebral blood flowMean arterial blood pressureEndothelium-derived nitric oxideTP receptor agonist UAbsence of NOCerebral circulatory parametersLow-frequency spontaneous fluctuationsArterial blood pressureTP receptor activationCerebrovascular toneEndothelial dysfunctionBlood pressureL-NAMEVascular effectsAgonist UNO deficiencyCirculatory parametersPharmacological modulationBlood flow
2007
Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice
Tirziu D, Chorianopoulos E, Moodie KL, Palac RT, Zhuang ZW, Tjwa M, Roncal C, Eriksson U, Fu Q, Elfenbein A, Hall AE, Carmeliet P, Moons L, Simons M. Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice. Journal Of Clinical Investigation 2007, 117: 3188-3197. PMID: 17975666, PMCID: PMC2045601, DOI: 10.1172/jci32024.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenic ProteinsAnimalsCardiomegalyCells, CulturedEchocardiographyEndothelial CellsEnzyme InhibitorsHeartHemodynamicsMiceMice, Inbred C57BLMice, TransgenicMyocardiumMyocytes, CardiacNeovascularization, PhysiologicNG-Nitroarginine Methyl EsterOrgan SizeRatsRats, Sprague-DawleyTransgenesConceptsMyocardial hypertrophyHeart sizeNormal heart sizeENOS inhibitor L-NAMEInhibitor L-NAMEAtrial natriuretic factorHypertrophic marker expressionNormal adult mouse heartAdult mouse heartAngiogenic growth factorsL-NAMEBeta-MHCCardiac massMyocardial infarctionMyocardial functionNatriuretic factorCardiac performanceCardiomyocyte sizeTransgenic miceStimulation periodHeart growthHypertrophy markersMarker expressionMouse heartsMurine heartFetal nucleated red blood cells in a rat model of intrauterine growth restriction induced by hypoxia and nitric oxide synthase inhibition
Ravishankar V, Buhimschi CS, Booth CJ, Bhandari V, Norwitz E, Copel J, Buhimschi IA. Fetal nucleated red blood cells in a rat model of intrauterine growth restriction induced by hypoxia and nitric oxide synthase inhibition. American Journal Of Obstetrics And Gynecology 2007, 196: 482.e1-482.e8. PMID: 17466713, DOI: 10.1016/j.ajog.2006.12.020.Peer-Reviewed Original ResearchConceptsIntrauterine growth restrictionNucleated red blood cellsNitric oxide inhibitionFetal nucleated red blood cellsChronic hypoxiaL-NAMEErythropoietin levelsOxide inhibitionRed blood cellsFetal circulationGrowth restrictionFetal bloodHematocrit levelsNumber of NRBCsNitro-L-arginine methyl esterChronic nitric oxide inhibitionMaternal acid-base statusNitric oxide synthase inhibitionBlood cellsMaternal arterial blood gasesOxide synthase inhibitionArterial blood gasesSaline solutionAdult Sprague-DawleyElevated erythropoietin levelsContrasting effects of chronic hypoxia and nitric oxide synthase inhibition on circulating angiogenic factors in a rat model of growth restriction
Bahtiyar MO, Buhimschi C, Ravishankar V, Copel J, Norwitz E, Julien S, Guller S, Buhimschi IA. Contrasting effects of chronic hypoxia and nitric oxide synthase inhibition on circulating angiogenic factors in a rat model of growth restriction. American Journal Of Obstetrics And Gynecology 2007, 196: 72.e1-72.e6. PMID: 17240241, DOI: 10.1016/j.ajog.2006.07.048.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChronic DiseaseDisease Models, AnimalEnzyme InhibitorsFemaleFetal Growth RetardationHypoxiaNG-Nitroarginine Methyl EsterNitric Oxide SynthasePlacenta Growth FactorPregnancyPregnancy ProteinsRatsRats, Sprague-DawleyVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth FactorsConceptsVascular endothelial growth factorL-NAMESerum levelsChronic hypoxiaSoluble fms-like tyrosine kinase-1Nitro-L-arginine methyl esterFms-like tyrosine kinase-1Adult Sprague-Dawley ratsGrowth factorMaternal serum levelsFree serum levelsIntrauterine growth restrictionOnset of laborPlacental growth factorTyrosine kinase-1Subcutaneous osmotic pumpsSprague-Dawley ratsNitric oxide inhibitionEndothelial growth factorNonpregnant controlsSFlt-1Growth restrictionHypoxic chamberMaternal bloodOxide inhibitionAcute tissue-type plasminogen activator release in human microvascular endothelial cells: The roles of Gαq, PLC-β, IP3 and 5,6-epoxyeicosatrienoic acid
Muldowney JA, Painter CA, Sanders-Bush E, Brown NJ, Vaughan DE. Acute tissue-type plasminogen activator release in human microvascular endothelial cells: The roles of Gαq, PLC-β, IP3 and 5,6-epoxyeicosatrienoic acid. Thrombosis And Haemostasis 2007, 97: 263-271. PMID: 17264956, DOI: 10.1160/th05-02-0092.Peer-Reviewed Original ResearchMeSH Keywords8,11,14-Eicosatrienoic AcidAortaBiological FactorsCell ProliferationCells, CulturedDose-Response Relationship, DrugEndothelial CellsEpoprostenolGTP-Binding Protein alpha Subunits, Gq-G11HumansInositol 1,4,5-TrisphosphateIsoenzymesMicrocirculationNitric OxidePhospholipase C betaPotassiumSignal TransductionThrombinTime FactorsTissue Plasminogen ActivatorType C PhospholipasesUmbilical VeinsConceptsT-PA releaseHuman microvascular endothelial cellsMicrovascular endothelial cellsEpoxyeicosatrienoic acidsTissue-type plasminogen activatorTissue-type plasminogen activator releaseEndothelial cellsIP3 receptor antagonistCalcium signalingT-PA antigenRole of GαqPlasminogen activator releaseMS-PPOHPhysiologic releaseCytochrome P450 inhibitorsL-NAMEEET antagonistReceptor antagonistActivator releaseVascular homeostasisNitric oxideProstacyclinPlasminogen activatorEET-methyl esterMicroM concentration
2005
Xanthine oxidase, nitric oxide synthase and phospholipase A2 produce reactive oxygen species via mitochondria
Sanganahalli B, Joshi P, Joshi N. Xanthine oxidase, nitric oxide synthase and phospholipase A2 produce reactive oxygen species via mitochondria. Brain Research 2005, 1037: 200-203. PMID: 15777770, DOI: 10.1016/j.brainres.2005.01.013.Peer-Reviewed Original ResearchConceptsMitochondrial depolarizationReactive oxygen speciesReactive oxygen species formationROS formationGlutamate-induced oxidative stressOxygen speciesDepolarized mitochondriaCytoplasmic enzymeFormation of reactive oxygen speciesNitric oxide synthaseRat cortical slicesL-NAMEMitochondriaPhospholipase A(2Presence of allopurinolSpeciesEnzymeAssociated with excitotoxicityCortical slicesPLA(2PhospholipasePhospholipase A2Xanthine oxidaseSynthaseOxidative stress
2004
NO Synthase Inhibition Increases Aldosterone in Humans
Muldowney JA, Davis SN, Vaughan DE, Brown NJ. NO Synthase Inhibition Increases Aldosterone in Humans. Hypertension 2004, 44: 739-745. PMID: 15381675, DOI: 10.1161/01.hyp.0000143852.48258.f1.Peer-Reviewed Original ResearchConceptsL-NAME infusionL-NAMEL-arginineAldosterone concentrationSerum potassiumNitro-L-arginine methyl esterNO precursor L-arginineEndogenous NO modulatesDouble-blind treatmentPlasma renin activityAngiotensin II concentrationEnzyme inhibitor ramiprilSystolic blood pressurePrecursor L-arginineRenin activityPlacebo pretreatmentBlood pressureSerum aldosteroneTreatment armsNO modulatesVehicle infusionHeart rateNormal subjectsSeparate daysCombined treatment
2002
Potential Roles of Plasminogen Activator System in Coronary Vascular Remodeling Induced by Long-term Nitric Oxide Synthase Inhibition
Kaikita K, Schoenhard JA, Painter CA, Ripley RT, Brown NJ, Fogo AB, Vaughan DE. Potential Roles of Plasminogen Activator System in Coronary Vascular Remodeling Induced by Long-term Nitric Oxide Synthase Inhibition. Journal Of Molecular And Cellular Cardiology 2002, 34: 617-627. PMID: 12054849, DOI: 10.1006/jmcc.2002.2001.Peer-Reviewed Original ResearchConceptsSystolic blood pressureNitric oxide synthase inhibitionOxide synthase inhibitionPerivascular fibrosisBlood pressurePAI-1 deficiencyCoronary perivascular fibrosisPlasminogen activator systemL-NAMENOS inhibitionSynthase inhibitionDeficient miceVascular pathologyLong-term nitric oxide synthase inhibitionNitro-L-arginine methyl esterL-NAME-induced hypertensionLong-term NOS inhibitionPlasma TGF-beta1 levelsPlasminogen activator inhibitor-1-deficient miceStructural vascular changesTGF-beta1 levelsLong-term treatmentTissue-type plasminogen activator-deficient miceWeek study periodActivator system
2001
Efficacy of intracoronary or intravenous VEGF165 in a pig model of chronic myocardial ischemia
Sato K, Wu T, Laham R, Johnson R, Douglas P, Li J, Sellke F, Bunting S, Simons M, Post M. Efficacy of intracoronary or intravenous VEGF165 in a pig model of chronic myocardial ischemia. Journal Of The American College Of Cardiology 2001, 37: 616-623. PMID: 11216988, DOI: 10.1016/s0735-1097(00)01144-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCoronary CirculationDose-Response Relationship, DrugEndothelial Growth FactorsEndothelium, VascularInfusions, Intra-ArterialInfusions, IntravenousLymphokinesMaleMicrocirculationMyocardial ContractionMyocardial IschemiaSwineVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsChronic myocardial ischemiaMyocardial ischemiaL-NAMEIntracoronary groupBlood flowNitro-L-arginine methyl ester hydrochlorideNitric oxide synthase inhibitionEndothelial growth factor treatmentLeft circumflex coronary arteryDose-limiting hypotensionOxide synthase inhibitionCircumflex coronary arteryVascular endothelial growth factor treatmentMyocardial blood flowRegional myocardial functionGrowth factor treatmentVEGF-induced angiogenesisIntravenous groupConcomitant administrationMicrovascular functionIntracoronary infusionCollateral indexDifferent regimensCoronary arteryIntravenous infusion
2000
Defective fluid and HCO3 − absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice
Wang T, Inglis F, Kalb R. Defective fluid and HCO3 − absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice. American Journal Of Physiology. Renal Physiology 2000, 279: f518-f524. PMID: 10966931, DOI: 10.1152/ajprenal.2000.279.3.f518.Peer-Reviewed Original ResearchMeSH KeywordsAcid-Base EquilibriumAnimalsBicarbonatesBiological TransportBlood Gas AnalysisBody FluidsElectrolytesEnzyme InhibitorsInjections, IntravenousKidney Tubules, ProximalMiceMice, Inbred C57BLMice, KnockoutNG-Nitroarginine Methyl EsterNitric Oxide SynthaseNitric Oxide Synthase Type IPotassiumSodiumConceptsNNOS knockout miceWild-type miceL-NAMEProximal tubulesMetabolic acidosisAbsorption of fluidDecreased absorption of fluidBlood pressureIncreased mean blood pressureResponse to L-NAMEWild-type control animalsFluid absorptionAdministration of L-NAMEIn situ microperfusionProximal tubule transportNeuronal nitric oxide synthaseLuminal perfusion solutionMean blood pressureRenal clearance techniquesNitric oxide synthaseRates of HCO(3)(-Urinary Na(+HCO3- absorptionRegulation of acid-base balanceTubule transport
1998
Nitric oxide increases the activity of the apical 70-pS K+ channel in TAL of rat kidney
Lu M, Wang X, Wang W. Nitric oxide increases the activity of the apical 70-pS K+ channel in TAL of rat kidney. American Journal Of Physiology 1998, 274: f946-f950. PMID: 9612333, DOI: 10.1152/ajprenal.1998.274.5.f946.Peer-Reviewed Original ResearchConceptsThick ascending limbNitric oxide synthaseNitric oxideRat kidneyL-NAMEL-NAME-induced inhibitionL-arginine methyl esterChannel activityMedullary thick ascending limbEffect of NOEffect of SNAPMM L-argininePatch-clamp techniqueCGMP-dependent pathwayD-NAMECell-attached patchesAngiotensin IIMicroM SNAPNOS activityOxide synthaseL-arginineAscending limbHenle's loopNO donorCGMP concentration
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply