0000000000206885

AUTHOR

Cristina Nuñez

showing 5 related works from this author

Discrepancies Between Nitroglycerin and NO-Releasing Drugs on Mitochondrial Oxygen Consumption, Vasoactivity, and the Release of NO

2005

It has been generally acknowledged that the actions of glyceryl trinitrate (GTN) are a result of its bioconversion into NO. However, recent observations have thrown this idea into doubt, with many studies demonstrating that NO is present only when there are high concentrations of GTN. We have explored this discrepancy by developing a new approach that uses confocal microscopy to directly detect NO. Intracellular levels of NO in the rat aortic vascular wall have been compared with those present after incubation with 3 different NO donors (DETA-NO, 3-morpholinosydnonimine, and S -nitroso- N -acetylpenicillamine), endothelial activation with acetylcholine, or administration of GTN. We have al…

MaleVascular smooth musclePhysiology:CIENCIAS MÉDICAS ::Farmacodinámica [UNESCO]In Vitro TechniquesPharmacologyMitochondrionNitric OxideGlyceryl trinitrateNitric oxideRats Sprague-DawleyNitroglycerinchemistry.chemical_compoundOxygen ConsumptionVascular relaxationGlyceryl trinitrate ; Nitric oxide ; Mitochondria ; Vascular relaxation ; NO donorsmedicineAnimalsCytochrome c oxidaseNitric Oxide DonorsMicroscopy ConfocalbiologyNO donorsNitric oxide:CIENCIAS MÉDICAS [UNESCO]AcetylcholineMitochondriaRatsVasodilationUNESCO::CIENCIAS MÉDICAS ::FarmacodinámicachemistryBiochemistryUNESCO::CIENCIAS MÉDICAScardiovascular systembiology.proteinLiberationCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseAcetylcholineIntracellularmedicine.drugCirculation Research
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Regulation of Oxygen Distribution in Tissues by Endothelial Nitric Oxide

2009

Nitric oxide (NO) decreases cellular oxygen (O 2 ) consumption by competitively inhibiting cytochrome c oxidase. Here, we show that endogenously released endothelial NO, either basal or stimulated, can modulate O 2 consumption both throughout the thickness of conductance vessels and in the microcirculation. Furthermore, we have shown that such modulation regulates O 2 distribution to the surrounding tissues. We have demonstrated these effects by measuring O 2 consumption in blood vessels in a hypoxic chamber and O 2 distribution in the microcirculation using the fluorescent oxygen-probe Ru(phen) 3 2+ . Removal of NO by physical or pharmacological means, or in eNOS −/− mice, abolishes this …

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologychemistry.chemical_elementOxygen consumptionBiologyNitric OxideOxygenMicrocirculationNitric oxideElectron Transport Complex IVRats Sprague-DawleyMicechemistry.chemical_compoundOxygen Consumption:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]EnosInternal medicinemedicineAnimalsHumansCytochrome c oxidaseEndotheliumHypoxiaUNESCO::CIENCIAS MÉDICAS ::Medicina internaMice KnockoutNitric Oxide Synthase Type IIINitric oxide:CIENCIAS MÉDICAS [UNESCO]biology.organism_classificationRatsOxygenEndocrinologymedicine.anatomical_structurechemistryUNESCO::CIENCIAS MÉDICASCirculatory systemBiophysicsbiology.proteinNitric oxide ; Endothelium ; Oxygen consumptionEndothelium VascularCardiology and Cardiovascular MedicineSignal TransductionCirculation Research
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Evaluation of the cytotoxic effects of MEIC chemicals 31-50 on primary culture of rat hepatocytes and hepatic and non-hepatic cell lines

1997

The cytotoxicities of 20 chemicals (numbers 31–50) from the Multicenter Evaluation of In Vitro Cytotoxicity (MEIC) programme were assessed with a primary culture of rat hepatocytes and with two hepatic cell lines (Hep G2 and FaO) and one non-hepatic cell line (3T3). The cytotoxicities of the chemicals were evaluated by using the MTT test after the cells had been exposed to the chemicals for 24 hours. For a better evaluation of results, dose–response curves were mathematically linearised and cytotoxicity was expressed as IC50 values and IC10 values (the concentration causing 50% and 10% loss of cell viability, respectively). We found that all the compounds showed similar acute basal cytotox…

General MedicinePharmacologyBiologyToxicologyGeneral Biochemistry Genetics and Molecular BiologyIn vitroHep G2Medical Laboratory Technologymedicine.anatomical_structureCell cultureHepatocyteImmunologyToxicityHepatic stellate cellmedicineCytotoxic T cellCytotoxicity
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Role of endothelial nitric oxide in pulmonary and systemic arteries during hypoxia

2014

Abstract Our aim was to investigate the role played by endothelial nitric oxide (NO) during acute vascular response to hypoxia, as a modulator of both vascular tone (through guanylate cyclase (sGC) activation) and mitochondrial O2 consumption (through competitive inhibition of cytochrome-c-oxydase (CcO)). Organ bath experiments were performed and O2 consumption (Clark electrode) was determined in isolated aorta, mesenteric and pulmonary arteries of rats and eNOS-knockout mice. All pre-contracted vessels exhibited a triphasic hypoxic response consisting of an initial transient contraction (not observed in vessels from eNOS-knockout mice) followed by relaxation and subsequent sustained contra…

MaleCancer ResearchContraction (grammar)Nitric Oxide Synthase Type IIIEndotheliumPhysiologyClinical BiochemistryVasodilationPulmonary ArteryMitochondrionPharmacologyNitric OxideBiochemistryNitric oxideRats Sprague-DawleyMicechemistry.chemical_compoundNon-competitive inhibitionEnosmedicineAnimalsHypoxiaAortaMice KnockoutbiologyMyxothiazolEndothelial Cellsbiology.organism_classificationMesenteric ArteriesRatsMice Inbred C57BLmedicine.anatomical_structurechemistryAnesthesiacardiovascular systemNitric Oxide
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Complex I dysfunction and tolerance to nitroglycerin: an approach based on mitochondrial-targeted antioxidants.

2006

Nitroglycerin (GTN) tolerance was induced in vivo (rats) and in vitro (rat and human vessels). Electrochemical detection revealed that the incubation dose of GTN (5×10 −6 mol/L) did not release NO or modify O 2 consumption when administered acutely. However, development of tolerance produced a decrease in both mitochondrial O 2 consumption and the K m for O 2 in animal and human vessels and endothelial cells in a noncompetitive action. GTN tolerance has been associated with impairment of GTN biotransformation through inhibition of aldehyde dehydrogenase (ALDH)-2, and with uncoupling of mitochondrial respiration. Feeding rats with mitochondrial-targeted antioxidants (mitoquinone [MQ]) and i…

MaleantioxidantAntioxidantPhysiologyUbiquinonemedicine.medical_treatmentMuscle RelaxationVasodilator AgentsAldehyde dehydrogenasePharmacologyMitochondrionmedicine.disease_causeAntioxidantsMuscle Smooth VascularRats Sprague-Dawleychemistry.chemical_compoundNitroglycerinDrug toleranceoxidative stressCyclic GMPchemistry.chemical_classificationbiologyAldehyde Dehydrogenase MitochondrialDrug ToleranceGlutathioneMitochondriamitochondriaBiochemistrycardiovascular systemCardiology and Cardiovascular Medicinecirculatory and respiratory physiologyMuscle ContractionendotheliumIn Vitro TechniquesMitochondrial ProteinsOrganophosphorus CompoundsOxygen ConsumptionRespirationmedicineAnimalsHumansReactive oxygen speciesElectron Transport Complex IDose-Response Relationship DrugEndothelial CellsGlutathioneAldehyde DehydrogenasenitroglycerinRatsOxidative Stresschemistrybiology.proteinReactive Oxygen SpeciesOxidative stressCirculation research
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