Search results for "Vascular"

showing 10 items of 10708 documents

Abacavir Increases Purinergic P2X7 Receptor Activation by ATP: Does a Pro-inflammatory Synergism Underlie Its Cardiovascular Toxicity?

2021

16 p.-9 fig.-1 tab.

0301 basic medicineAgonistAllosteric modulatormedicine.drug_classAllosteric modulatoradenosine triphosphateAllosteric regulationPharmacologyleukocyte-endothelium interactionsProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineimmune system diseasesAbacavirmedicinePharmacology (medical)Original ResearchPharmacologyApyraseLeukocyte-endothelium interactionsabacavirlcsh:RM1-950Purinergic receptorallosteric modulatorvirus diseasesAbacavircardiovascular diseasesCardiovascular diseaseslcsh:Therapeutics. Pharmacology030104 developmental biologychemistryP2X7 receptorAdenosine triphosphate030217 neurology & neurosurgeryAdenosine triphosphatemedicine.drugFrontiers in Pharmacology
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Muscarinic type-1 receptors contribute to I-K,I-ACh in human atrial cardiomyocytes and are upregulated in patients with chronic atrial fibrillation

2018

Background: Basal and acetylcholine-gated inward-rectifier K+-currents (I-K1 and I-K,I-ACh, respectively) are altered in atrial fibrillation (AF). G(i)-protein-coupled muscarinic (M) receptors type-2 are considered the predominant receptors activating I-K,I-ACh. Although a role for G(q)-coupled non-M-2-receptor subtypes has been suggested, the precise regulation of I-K,I-ACh by multiple M-receptor subtypes in the human atrium is unknown. Here, we investigated M-1-receptor-mediated I-K,I-ACh regulation and its remodeling in chronic AF (cAF). Methods and results: M-1-receptor mRNA and protein abundance were increased in atrial cardiomyocyte fractions and atrial homogenates from cAF patients, …

0301 basic medicineAgonistEXPRESSIONmedicine.medical_specialtyCarbacholmedicine.drug_classMedizin030204 cardiovascular system & hematologyPertussis toxinSUBTYPES03 medical and health sciences0302 clinical medicineInternal medicineMuscarinic acetylcholine receptormedicinePROTEIN-KINASE-CReceptorAcetylcholine receptorK+-CURRENTACETYLCHOLINE-RECEPTORSCHANNELSCONGESTIVE-HEART-FAILUREbusiness.industryMuscarinic receptor subtypesInward-rectifier K+-channelELECTROPHYSIOLOGYPirenzepineAtrial fibrillationDEPENDENT REGULATIONPOTASSIUM CURRENTS030104 developmental biologyEndocrinologyCardiology and Cardiovascular MedicinebusinessAcetylcholinemedicine.drug
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Glucagon-like peptide-1 (GLP-1) receptor agonists and their cardiovascular benefits-The role of the GLP-1 receptor.

2021

Cardiovascular outcome trials revealed cardiovascular benefits for type 2 diabetes mellitus patients when treated with long-acting glucagon-like peptide-1 (GLP-1) receptor agonists. In the last decade, major advances were made characterising the physiological effects of GLP-1 and its action on numerous targets including brain, liver, kidney, heart and blood vessels. However, the effects of GLP-1 and receptor agonists, and the GLP-1 receptor on the cardiovascular system have not been fully elucidated. We compare results from cardiovascular outcome trials of GLP-1 receptor agonists and review pleiotropic clinical and preclinical data concerning cardiovascular protection beyond glycaemic contr…

0301 basic medicineAgonistendocrine systemmedicine.drug_classDiseasePharmacologyCardiovascular SystemGlucagon-Like Peptide-1 Receptor03 medical and health sciences0302 clinical medicineGlucagon-Like Peptide 1Diabetes mellitusMedicineHumansHypoglycemic AgentsReceptorGlucagon-like peptide 1 receptorPharmacologyKidneybusiness.industrydigestive oral and skin physiologyType 2 Diabetes Mellitusmedicine.diseaseGlucagon-like peptide-1030104 developmental biologymedicine.anatomical_structureDiabetes Mellitus Type 2Cardiovascular Diseasesbusinesshormones hormone substitutes and hormone antagonists030217 neurology & neurosurgeryBritish journal of pharmacology
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Estradiol, acting through ERα, induces endothelial non-classic renin-angiotensin system increasing angiotensin 1–7 production

2016

Intracellular renin-angiotensin system (RAS) can operate independently of the circulating RAS. Estrogens provide protective effects by modulating the RAS. Our aim was to investigate the effect of estradiol (E2) on angiotensin converting enzymes (ACE) 1 and ACE2 expression and activities in human endothelial cells (HUVEC), and the role of estrogen receptors (ER). The results confirmed the presence of active intracellular RAS in HUVEC. Physiological concentrations of E2 induced a concentration-dependent increase of ACE1 and ACE2 mRNA expression and ACE1, but not ACE2, protein levels. ACE1 and ACE2 enzymatic activities were also induced with E2. These effects were mediated through ERα activati…

0301 basic medicineAgonistmedicine.medical_specialtymedicine.drug_classEstrogen receptorPeptidyl-Dipeptidase A030204 cardiovascular system & hematologyBiologyBiochemistryEstrogen Receptor AntagonistsCiencias Biológicas03 medical and health sciences0302 clinical medicineEndocrinologyPiperidinesInternal medicineRenin–angiotensin systemHuman Umbilical Vein Endothelial CellsmedicineHumansFulvestrantMolecular BiologyESTROGEN RECEPTORDose-Response Relationship DrugEstradiolEstrogen Receptor alphaANGIOTENSIN CONVERTING ENZYMESBioquímica y Biología MolecularRENIN ANGIOTENSIN SYSTEMPeptide FragmentsEndothelial stem cellESTROGEN030104 developmental biologyEndocrinologyGene Expression RegulationEstrogenENDOTHELIAL CELLPyrazolesAngiotensin-Converting Enzyme 2Estrogen Receptor AntagonistsAngiotensin IEstrogen receptor alphaCIENCIAS NATURALES Y EXACTAShormones hormone substitutes and hormone antagonistsIntracellularMolecular and Cellular Endocrinology
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Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension

2020

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidati…

0301 basic medicineAircraftmedicine.medical_treatmentClinical BiochemistryBlood Pressure1308 Clinical Biochemistrymedicine.disease_causeBiochemistryMice0302 clinical medicineMedicineEndothelial dysfunctionlcsh:QH301-705.5lcsh:R5-920NADPH oxidasebiologyCytokineHypertensionmedicine.symptomlcsh:Medicine (General)Arterial hypertensionmedicine.medical_specialtyArticles from the Special Issue on Impact of environmental pollution and stress on redox signaling and oxidative stress pathways; Edited by Thomas Münzel and Andreas Daiber10208 Institute of Neuropathology610 Medicine & healthInflammation03 medical and health sciencesInternal medicineEnvironmental noise exposureAnimalsNeuroinflammationInflammationbusiness.industryOrganic ChemistryEndothelial functionmedicine.diseaseAngiotensin IIMice Inbred C57BLOxidative Stress030104 developmental biologyEndocrinologyBlood pressurelcsh:Biology (General)Vascular oxidative stressbiology.protein570 Life sciences; biologyEndothelium Vascularbusiness030217 neurology & neurosurgeryOxidative stress1605 Organic ChemistryRedox Biology
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Vascular biotransformation of organic nitrates is independent of cytochrome P450 monooxygenases

2020

Background and Purpose Organic nitrates such as nitroglycerin (NTG) or pentaerythritol tetranitrate (PETN) have been used for over a century in the treatment of angina or ischaemic heart disease. These compounds are prodrugs which release their nitrovasodilators upon enzymic bioactivation by aldehyde dehydrogenase (ALDH2) or cytochromes P450 (CYP). Whereas ALDH2 is known to directly activate organic nitrates in vessels, the contribution of vascular CYPs is unknown and was studied here. Experimental Approach As all CYPs depend on cytochrome P450 reductase (POR) as electron donor, we generated a smooth muscle cell-specific, inducible knockout mouse of POR (smcPOR−/−) to investigate the contri…

0301 basic medicineAldehyde dehydrogenasePharmacologyMiceNitroglycerin03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCytochrome P-450 Enzyme SystemAnimalsPentaerythritol Tetranitrateddc:610NitriteBiotransformationVascular tissuePharmacologyNitratesbiologyChemistryCytochrome P450Cytochrome P450 reductaseMetabolismMonooxygenase030104 developmental biologybiology.proteinMicrosome030217 neurology & neurosurgeryBritish Journal of Pharmacology
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Direct Sensing of Nutrients via a LAT1-like Transporter in Drosophila Insulin-Producing Cells

2016

Summary Dietary leucine has been suspected to play an important role in insulin release, a hormone that controls satiety and metabolism. The mechanism by which insulin-producing cells (IPCs) sense leucine and regulate insulin secretion is still poorly understood. In Drosophila, insulin-like peptides (DILP2 and DILP5) are produced by brain IPCs and are released in the hemolymph after leucine ingestion. Using Ca2+-imaging and ex vivo cultured larval brains, we demonstrate that IPCs can directly sense extracellular leucine levels via minidiscs (MND), a leucine transporter. MND knockdown in IPCs abolished leucine-dependent changes, including loss of DILP2 and DILP5 in IPC bodies, consistent wit…

0301 basic medicineAmino Acid Transport Systemsheavy-chainmedicine.medical_treatmentInsulinsamino acid transporter0302 clinical medicinegenetics [Drosophila Proteins]cytology [Drosophila melanogaster]Glutamate DehydrogenaseHemolymphInsulin-Secreting Cellsmetabolism [Drosophila melanogaster]HemolymphDrosophila;Drosophila insulin-like peptides;amino acid transporter;food;glutamate dehydrogenase;glycemia;growth;insulin-producing cells;minidiscs;starvationDrosophila ProteinsProtein Isoformsmetabolism [Calcium]genetics [Insulins]genetics [Amino Acid Transport Systems]lcsh:QH301-705.5minidiscsGene knockdowncytology [Larva]pancreatic beta-cellglutamate dehydrogenaseBrainmetabolism [Hemolymph]secretionDrosophila melanogasterBiochemistryLarvaAlimentation et NutritionDrosophilaLeucineSignal Transductionglucose-transportgenetics [Glutamate Dehydrogenase]genetics [Protein Isoforms]growthamino-acidsmetabolism [Drosophila Proteins][SDV.BC]Life Sciences [q-bio]/Cellular BiologyNutrient sensingmetabolism [Larva]Biologyinsulin-producing cellsArticleGeneral Biochemistry Genetics and Molecular Biologymetabolism [Amino Acid Transport Systems]metabolism [Insulins]03 medical and health sciencesLeucineparasitic diseasesmedicineFood and NutritionAnimalsddc:610cytology [Insulin-Secreting Cells]cardiovascular diseasesAmino acid transporterMnd protein Drosophilaadministration & dosage [Leucine]metabolism [Protein Isoforms]Ilp5 protein Drosophilacytology [Brain]foodGlutamate dehydrogenaseInsulinNeurosciencesstarvationGlucose transportermetabolism [Insulin-Secreting Cells]glutamate-dehydrogenasel-leucineglycemia030104 developmental biologyGene Expression Regulationlcsh:Biology (General)metabolism [Brain]metabolism [Glutamate Dehydrogenase]Neurons and Cognitionmetabolism [Leucine]CalciumDrosophila insulin-like peptidesmetabolismfat-cells030217 neurology & neurosurgeryCell Reports
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Maternal and fetal genetic contribution to gestational weight gain

2018

Background: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG. Participants and methods: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspri…

0301 basic medicineAmniotic fluidEpidemiologyEndocrinology Diabetes and MetabolismEmbaràsMedicine (miscellaneous)Genome-wide association studyBLOOD-PRESSUREType 2 diabetes030204 cardiovascular system & hematology/dk/atira/pure/core/keywords/icepCOMMON SNPSGenètica mèdica0302 clinical medicinePregnancyWeight managementOFFSPRING ADIPOSITYMass index11 Medical and Health Sciences2. Zero hunger0303 health sciencesNutrition and DieteticsObstetricsHERITABILITYMedical geneticsta3141ASSOCIATIONGestational Weight Gainddc:3. Good healthGestational diabetesCHILDREN ALSPACmedicine.anatomical_structurePREGNANCYOBESITYMENDELIAN RANDOMIZATIONGestationOriginal ArticleFemaleICEPmedicine.symptomLife Sciences & Biomedicine13 EducationTRAITSmedicine.medical_specialtyOffspringBirth weightPes corporalDevelopmentBiology03 medical and health sciencesEndocrinology & MetabolismFetusPlacentaInternal medicinemedicineJournal ArticleHumans030304 developmental biologyFetusPregnancyScience & TechnologyNutrition & Dieteticsbusiness.industryta3121Body weightmedicine.diseaseta3123BIRTH-WEIGHTBODY-MASS INDEX030104 developmental biologyEndocrinologybusinessBody mass indexWeight gainHUMAN HEIGHTGenome-Wide Association Study
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Platelet Pathogen Reduction Technologies Alter the MicroRNA Profile of Platelet-Derived Microparticles

2020

Despite improvements in donor screening and increasing efforts to avoid contamination and the spread of pathogens in clinical platelet concentrates (PCs), the risks of transfusion-transmitted infections remain important. Relying on an ultraviolet photo activation system, pathogen reduction technologies (PRTs), such as Intercept and Mirasol, utilize amotosalen, and riboflavin (vitamin B2), respectively, to mediate inactivation of pathogen nucleic acids. Although they are expected to increase the safety and prolong the shelf life of clinical PCs, these PRTs might affect the quality and function of platelets, as recently reported. Upon activation, platelets release microparticles (MPs), which …

0301 basic medicineAmotosalenmedicine.medical_specialtySmall RNAlcsh:Diseases of the circulatory (Cardiovascular) systemmirasolCardiovascular Medicine030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineclinical platelet concentrateInternal medicinemicroRNAmedicinePlateletHematologiPathogenOriginal ResearchRegulation of gene expressionHematologymicroRNApathogen reductionChemistryclinical platelet concentrate; pathogen reduction; mirasol; intercept; extracellular vesicles; small RNA-sequencing; microRNAHematology3. Good healthCell biologysmall RNA-sequencing030104 developmental biologylcsh:RC666-701extracellular vesiclesCardiology and Cardiovascular MedicineFunction (biology)interceptFrontiers in Cardiovascular Medicine
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Cellular and Molecular Heterogeneity Associated with Vessel Formation Processes

2018

The microvasculature heterogeneity is a complex subject in vascular biology. The difficulty of building a dynamic and interactive view among the microenvironments, the cellular and molecular heterogeneities, and the basic aspects of the vessel formation processes make the available knowledge largely fragmented. The neovascularisation processes, termed vasculogenesis, angiogenesis, arteriogenesis, and lymphangiogenesis, are important to the formation and proper functioning of organs and tissues both in the embryo and the postnatal period. These processes are intrinsically related to microvascular cells, such as endothelial and mural cells. These cells are able to adjust their activities in r…

0301 basic medicineAngiogenesisNeovascularization Physiologiclcsh:MedicineReview ArticleBiologyMolecular heterogeneityGeneral Biochemistry Genetics and Molecular BiologyMural cell03 medical and health sciences0302 clinical medicineVasculogenesisAnimalsHumansGeneral Immunology and Microbiologylcsh:RVascular biologyGeneral MedicineLymphangiogenesis030104 developmental biologyOrgan Specificity030220 oncology & carcinogenesisBlood VesselsArteriogenesisNeuroscienceSignal TransductionBioMed Research International
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