Search results for "Angiotensin II"

showing 10 items of 176 documents

PO-002 Angiotensin II-induced hypertension increases the mutation frequency in the rat kidney

2018

Introduction Epidemiological studies revealed an increased risk for kidney cancer in hypertensive patients. In many of these patients, the blood pressure regulating renin angiotensin aldosterone system (RAAS) is activated. A stimulated RAAS can lead to oxidative stress and DNA damage, as we have shown both in vitro and in animal models of hypertension. Here, we used a rat model to quantify mutations generated by 20 weeks of angiotensin II-infusion. Material and methods BigBlue+/- rats, which carry a transgenic lacI gene for mutation analysis, were treated with 0.4 mg angiotensin II/kg/day with the help of osmotic minipumps. Urinary samples were collected in week 15 by placing the rats into …

Cancer ResearchKidneymedicine.medical_specialtyDNA damagebusiness.industryUrinary systemmedicine.disease_causeAngiotensin IImedicine.anatomical_structureEndocrinologyOncologyInternal medicineRenal physiologyRenin–angiotensin systemmedicineMutation frequencybusinessOxidative stressESMO Open
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Regulation of endothelial-type NO synthase expression in pathophysiology and in response to drugs.

2002

In many types of cardiovascular pathophysiology such as hypercholesterolemia and atherosclerosis, diabetes, cigarette smoking, or hypertension (with its sequelae stroke and heart failure) the expression of endothelial NO synthase (eNOS) is altered. Both up- and downregulation of eNOS have been observed, depending on the underlying disease. When eNOS is upregulated, the upregulation is often futile and goes along with a reduction in bioactive NO. This is due to an increased production of superoxide generated by NAD(P)H oxidase and by an uncoupled eNOS. A number of drugs with favorable effects on cardiovascular disease upregulate eNOS expression. The resulting increase in vascular NO producti…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryPharmacologymedicine.disease_causeNitric OxideBiochemistrychemistry.chemical_compoundDownregulation and upregulationMetabolic DiseasesEnosInternal medicineDiabetes mellitusmedicineAnimalsHumansEndothelial dysfunctionAngiotensin II receptor type 1biologybusiness.industrySuperoxidemedicine.diseasebiology.organism_classificationEndocrinologychemistryGene Expression RegulationErythropoietinCardiovascular DiseasesNitric Oxide SynthasebusinessOxidative stressmedicine.drugNitric oxide : biology and chemistry
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Physiological mechanisms regulating the expression of endothelial-type NO synthase

2002

Although endothelial nitric oxide synthase (eNOS) is a constitutively expressed enzyme, its expression is regulated by a number of biophysical, biochemical, and hormonal stimuli, both under physiological conditions and in pathology. This review summarizes the recent findings in this field. Shear stress, growth factors (such as transforming growth factor-beta, fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor), hormones (such as estrogens, insulin, angiotensin II, and endothelin 1), and other compounds (such as lysophosphatidylcholine) upregulate eNOS expression. On the other hand, the cytokine tumor necrosis factor-alpha and bacterial lipopolys…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyRNA Stabilitymedicine.medical_treatmentClinical BiochemistryBiologyFibroblast growth factorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundEnosInternal medicinemedicineAnimalsPromoter Regions GeneticRegulation of gene expressionBase SequenceGene Expression ProfilingGrowth factorbiology.organism_classificationActin cytoskeletonAngiotensin IICell biologyVascular endothelial growth factorEndocrinologychemistryNitric Oxide SynthaseSignal transductionSignal TransductionNitric Oxide
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Procollagen C-Proteinase Enhancer 1 (PCPE-1) is a marker of myocardial fibrosis and impaired cardiac function in a murine model of pressure overload

2021

Abstract(1)AimsProcollagen C-proteinase enhancer 1 (PCPE-1) is an extracellular matrix protein and a major regulator of fibrillar collagen biosynthesis. Previous work has shown that its abundance is often increased in the context of tissue repair and fibrosis. The present study was designed to evaluate its potential as a biomarker of myocardial interstitial fibrosis (MIF), a well-established pathogenic pathway leading to heart failure.(2)Methods and ResultsCardiac fibrosis was induced in rats using an optimized model of chronic pressure overload triggered by angiotensin II and Nω-nitro-L-arginine methyl ester (L-NAME). All treated animals suffered from heart hypertrophy and the increase in …

Cardiac function curvemedicine.medical_specialtyCardiac fibrosis[SDV]Life Sciences [q-bio]Diastoleheart failure030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineFibrosisInternal medicinemedicine030304 developmental biologyPressure overload0303 health sciencesCardiac fibrosiscirculating biomarkerbusiness.industrycollagen biosynthesismedicine.diseaseProcollagen C-proteinase enhancer 1 (PCPE-1)Angiotensin IIEndocrinologyHeart failureMyocardial fibrosisPET-MR imagingbusiness
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Synergistic Effect of Carfilzomib and Metformin in Vascular Plasticity; The Emerging Role of Autophagy

2019

Introduction: Carfilzomib (Cfz) correlates with a risk of reversible cardiotoxicity in 5-10% of multiple myeloma (MM) patients. We have recently shown that metformin (Met) has a prophylactic role against the Cfz-induced cardiotoxicity in vivo, through activation of AMPKα signaling (Blood 2019;133:710-23). However, the impact of Cfz on vascular function is obscure. Therefore, we sought to investigate: i) the acute, ii) the sub-chronic effect of Cfz on the vascular reactivity, iii) the effect of metformin co-administration on the vascular phenotype and iv) the impact of Cfz and Met co-administration on aged Human Aortic Smooth Muscle Cells (HAoSMCs). Methods: Forty male C57Bl/6 mice were assi…

CardiotoxicityMulticatalytic endopeptidase complexbusiness.industryMTOR Serine-Threonine KinasesImmunologyAutophagyCell BiologyHematologyBiochemistryCarfilzomibAngiotensin IIMetforminchemistry.chemical_compoundchemistryAnimals laboratoryCancer researchmedicinebusinessmedicine.drugBlood
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Vergleichende reaktionskinetische Untersuchungen mit standardisiertem menschlichen Renin an vier angereicherten tierischen Reninsubstraten

1970

Zur Charakterisierung der Angiotensinbildung aus vier angereicherten tierischen Reninsubstraten (Rind, Schwein, Hund und Ratte) mit menschlichem Renin wurde das Temperatur- und pH-Verhalten untersucht, sowie die Michaelis-Menten-Konstanten und maximalen Reaktionsgeschwindigkeiten bestimmt.

Chemical kineticsPhysiologyChemistryPhysiology (medical)Clinical BiochemistryRenin–angiotensin systemHuman physiologyMolecular biologyAngiotensin IIHuman reninPfl�gers Archiv European Journal of Physiology
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Comparative study of capillary electroendosmotic chromatography and electrically assisted gradient nano-liquid chromatography for the separation of p…

2000

Capillary electroendoendosmotic chromatography (CEC), being a hybrid of high-performance liquid chromatography (HPLC) and capillary electrophoresis, offers considerable changes to enhance column efficiency, speed of analysis and additional selectivity as compared to the parent methods. The analytes are driven by the electroendosmotic flow (EOF) and separated by surface-solute interactions as well as by differences in electromigration. In this paper on the separation of peptides on C18 reversed-phase and mixed-mode (sulphonic acid-n-alkyl) packings in CEC and electrically assisted reversed-phase gradient nano-LC are investigated. It is shown that mixed mode packings generate a higher EOF tha…

ChromatographyElutionChemistryOrganic ChemistryAnalytical chemistryElectrophoresis CapillaryCytochrome c GroupGeneral MedicineReversed-phase chromatographyHydrogen-Ion ConcentrationBiochemistryHigh-performance liquid chromatographyAngiotensin IIAnalytical ChemistryCapillary electrophoresisColumn chromatographyMixed-mode chromatographyElectrochromatographyPeptidesChromatography High Pressure LiquidJournal of chromatography. A
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Extent and duration of angiotensin ii antagonistic activity of irbesartan and candesartan cilexetil

2000

Clinical pharmacologybusiness.industryPharmacologyAngiotensin IIlaw.inventionCandesartanIrbesartanLosartanValsartanlawRenin–angiotensin systemInternal Medicinemedicinebusinessmedicine.drugAmerican Journal of Hypertension
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Effects of Losartan and Delapril on the Fibrinolytic System in Patients with Mild to Moderate Hypertension

2007

Background and objectives: Angiotensin-converting enzyme (ACE) probably influences the fibrinolytic system at a central point by converting angiotensin I to angiotensin II, which increases plasminogen activator inhibitor-1 (PAI-1) activity. This effect appears to be mediated in humans via the angiotensin II type 1 (AT1) receptor. The objective of this study was to evaluate, in patients with mild to moderate hypertension, the change in tissue plasminogen activator (t-PA) and PAI-1 plasma levels after treatment with an AT1-receptor blocker (losartan 50 mg/day) or an ACE inhibitor (delapril 60 mg/day). Patients and methods: 30 hypertensive patients and 15 controls were enrolled. Essential hype…

Creatininemedicine.medical_specialtybiologybusiness.industryDelaprilAngiotensin-converting enzymeGeneral MedicineEssential hypertensionmedicine.diseaseAngiotensin IIGastroenterologychemistry.chemical_compoundEndocrinologyBlood pressureLosartanchemistryInternal medicineACE inhibitormedicinebiology.proteinPharmacology (medical)businessmedicine.drugClinical Drug Investigation
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Different effects of losartan and delapril on plasma PAI-1 levels in patients with mild to moderate hypertension

2003

ACE probably influences the fibrinolytic system at acentral point by converting angiotensin I to angiotensin II,which increases PAI-1 activity. This effect appears to bemediated via the AT1-receptor in humans. The RAAS mayalso contribute to a reduction in t-PA production by degra-dation of bradykinin, since the latter increases the release ofprostacyclin, nitric oxide, and t-PA from endothelial cells.Accordingly, ACE inhibitors not only influence the fibrino-lytic system by a reduction of PAI-1 activity but also byincreasing t-PA activity [1–3]. However, few studies haveanalysed the effects of AT1-R antagonists on t-PA and PAI-1plasma levels and the in vivo effects of AT1-R antagonistson th…

Creatininemedicine.medical_specialtybusiness.industryDelaprilEssential hypertensionmedicine.diseaseLeft ventricular hypertrophyAngiotensin IIGastroenterologychemistry.chemical_compoundEndocrinologyLosartanchemistryInternal medicineHeart failuremedicineMyocardial infarctionCardiology and Cardiovascular Medicinebusinessmedicine.drugInternational Journal of Cardiology
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