Search results for "angiotensin II"

showing 10 items of 176 documents

Combined treatment with bexarotene and rosuvastatin reduces angiotensin-II-induced abdominal aortic aneurysm in apoE−/−mice and angiogenesis

2015

Background and Purpose Abdominal aortic aneurysm (AAA) is a degenerative vascular disease associated with angiogenesis. Bexarotene is a retinoid X receptor (RXR) ligand with anti-angiogenic activity. Statins also exert anti-angiogenic activity and activate PPARs. Because RXR ligands form permissive heterodimers with PPARs and a single anti-angiogenic drug may not be sufficient to combat the wide array of angiogenic factors produced during AAA, we evaluated the effect of combined low doses of bexarotene and rosuvastatin in a mouse model of AAA.

PharmacologyBexaroteneAngiogenesisPharmacologyRetinoid X receptorBiologymedicine.diseaseenvironment and public healthAngiotensin IINeovascularizationAortic aneurysmRosuvastatin Calciumcardiovascular systemmedicinelipids (amino acids peptides and proteins)Rosuvastatincardiovascular diseasesmedicine.symptommedicine.drugBritish Journal of Pharmacology
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Effect of two phenanthrene alkaloids on angiotensin II-induced leukocyte-endothelial cell interactionsin vivo

2003

The present study has evaluated the effect of two phenanthrene alkaloids, uvariopsine and stephenanthrine, on angiotensin II (Ang-II)-induced leukocyte–endothelial cell interactions in vivo and the mechanisms involved in their activity. Intravital microscopy within the rat mesenteric microcirculation was used. A 60 min superfusion with 1 nM Ang-II induced a significant increase in the leukocyte–endothelial cell interactions that were completely inhibited by 1 μM uvariopsine cosuperfusion. A lower dose of 0.1 μM significantly reduced Ang-II-induced leukocyte adhesion by 75%. When Ang-II was cosuperfused with 1 and 0.1 μM stephenanthrine, Ang-II-induced leukocyte responses were significantly …

Pharmacologychemistry.chemical_classificationmedicine.medical_specialtyReactive oxygen speciesPlatelet-activating factorSuperoxideLeukocyte RollingPharmacologyN-Formylmethionine leucyl-phenylalanineAngiotensin IIEndothelial stem cellchemistry.chemical_compoundEndocrinologychemistryInternal medicinemedicineIntracellularBritish Journal of Pharmacology
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Angiotensin II is involved in nitric oxide synthase and cyclo-oxygenase inhibition-induced leukocyte-endothelialcell interactionsin vivo

2001

Chronic inhibition of nitric oxide synthase (NOS) provokes a hypertensive state which has been shown to be angiotensin II (Ang-II) dependent. In addition to raising blood pressure, NOS inhibition also causes leukocyte adhesion. The present study was designed to define the role of Ang-II in hypertension and in the leukocyte-endothelial cell interactions induced by acute NOS or cyclo-oxygenase (COX) inhibition using intravital microscopy within the rat mesenteric microcirculation. While pretreatment with an Ang-II AT1 receptor antagonist (losartan) reversed the prompt increase in mean arterial blood pressure (MABP) caused by indomethacin, it had no effect on the increase evoked by systemic L-…

Pharmacologymedicine.medical_specialtyAngiotensin II receptor type 1EndotheliumbiologyLeukocyte RollingProstacyclinAngiotensin IINitric oxideNitric oxide synthasechemistry.chemical_compoundLosartanmedicine.anatomical_structureEndocrinologychemistryInternal medicinecardiovascular systemmedicinebiology.proteinhormones hormone substitutes and hormone antagonistsmedicine.drugBritish Journal of Pharmacology
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Uncoupling of endothelial NO synthase in atherosclerosis and vascular disease.

2013

Nitric oxide (NO) produced by the endothelial NO synthase (eNOS) is an antihypertensive, antithrombotic and anti-atherosclerotic molecule. Hypercholesterolemia leads to a reduction in vascular NO bioavailability. This is attributed to a dysfunction of the eNOS enzyme and a reduced eNOS activity. NADPH oxidase-mediated oxidative stress leads to oxidation of tetrahydrobiopterin (BH4), the essential cofactor of eNOS. In BH4 deficiency, oxygen reduction uncouples from NO synthesis, thereby converting eNOS to a superoxide-producing enzyme. As a consequence of eNOS uncoupling, NO production is reduced and the pre-existing oxidative stress is enhanced, which contribute significantly to atherogenes…

Pharmacologymedicine.medical_specialtyAngiotensin II receptor type 1biologyNitric Oxide Synthase Type IIINitric Oxide Synthase Type IIITetrahydrobiopterinResveratrolbiology.organism_classificationmedicine.disease_causeNitric OxideNebivololNitric oxidechemistry.chemical_compoundEndocrinologychemistryEnosInternal medicineDrug DiscoverymedicineAnimalsHumansVascular DiseasesOxidative stressmedicine.drugCurrent opinion in pharmacology
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Zum Einfluss von Angiotensin II auf die Nebennierenrinde unter chemischer adrenostase mit SU 4885 (Metopiron)

1964

The inhibition of 11-β-hydroxylase in the adrenal cortex with SU 4885 (metopiron) increases the ACTH-secretion. Val5-angiotensin II blocks the reaction of the anterior pituitary gland similarly as does dexamethasone. Mode and intensity of this action of angiotensin II, and the influence on rats treated as described, are studied.

Pharmacologymedicine.medical_specialtyChemistryAdrenal cortexCell BiologyAngiotensin IICellular and Molecular Neurosciencemedicine.anatomical_structureEndocrinologyAnterior pituitaryInternal medicinemedicineMolecular MedicineMolecular BiologyDexamethasonemedicine.drugExperientia
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Modifications induced in the renin-angiotensin-aldo-sterone system of rats by alpha-blocking drugs.

1978

Summary The data reported in the present paper refer to quantitative variations of plasma renin activity and plasma aldosterone levels after administration of alpha-blocking agents, i.e. phentolamine, phenoxybenzamine and gihydroergotoxin derivatives, either to rats kept on a standard diet with water ad libitum or to rats receiving distilled water load, the latter treatment causing an increase of both plasma renin activity and plasma aldosterone levels if compared to control values. No strict correlation between (a) drug-induced modifications of plasma renin activity and plasma aldosterone levels and (b) blood pressure drop caused by the same drugs was shown to occur under either experiment…

Pharmacologymedicine.medical_specialtyChemistryPhenoxybenzamineAngiotensin IIBlood PressurePharmacologyPlasma renin activityBlood pressure dropRatsAlpha blockingPhentolamineEndocrinologyHigh plasmaInternal medicineRenin–angiotensin systemReninmedicineStandard dietAnimalsAldosteroneAdrenergic alpha-Antagonistsmedicine.drugPharmacological research communications
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Cyclic AMP elevating agents and nitric oxide modulate angiotensin II-induced leukocyte-endothelial cell interactionsin vivo

2001

Angiotensin (Ang-II) is a key molecule in the development of cardiac ischaemic disorders and displays proinflammatory activity in vivo. Since intracellular cyclic nucleotides elevating agents have proved to be effective modulators of leukocyte recruitment, we have evaluated their effect on Ang-II-induced leukocyte-endothelial cell interactions in vivo using intravital microscopy within the rat mesenteric microcirculation. Pretreatment with iloprost significantly inhibited (1 nM) Ang-II-induced increase in leukocyte rolling flux, adhesion and emigration at 60 min by 96, 92 and 90% respectively, and returned leukocyte rolling velocity to basal levels. Pretreatment with salbutamol or co-superf…

Pharmacologymedicine.medical_specialtyForskolinCell adhesion moleculeLeukocyte RollingBiologyAngiotensin IIEndothelial stem cellchemistry.chemical_compoundEndocrinologychemistryIn vivoInternal medicinemedicineRolipramIntravital microscopymedicine.drugBritish Journal of Pharmacology
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Molecular Mechanisms of the Crosstalk Between Mitochondria and NADPH Oxidase Through Reactive Oxygen Species—Studies in White Blood Cells and in Anim…

2014

Aims: Oxidative stress is involved in the development of cardiovascular disease. There is a growing body of evidence for a crosstalk between different enzymatic sources of oxidative stress. With the present study, we sought to determine the underlying crosstalk mechanisms, the role of the mitochondrial permeability transition pore (mPTP), and its link to endothelial dysfunction. Results: NADPH oxidase (Nox) activation (oxidative burst and translocation of cytosolic Nox subunits) was observed in response to mitochondrial reactive oxygen species (mtROS) formation in human leukocytes. In vitro, mtROS-induced Nox activation was prevented by inhibitors of the mPTP, protein kinase C, tyrosine kin…

PhysiologyNeutrophilsClinical BiochemistryBiologyMitochondrionmedicine.disease_causeBiochemistryModels BiologicalSuperoxide dismutaseCyclophilinsMiceForum Original Research CommunicationsMitochondria (A. Daiber Ed.)medicineLeukocytesAnimalsHumansMolecular BiologyGeneral Environmental ScienceRespiratory Burstchemistry.chemical_classificationMice KnockoutReactive oxygen speciesNADPH oxidaseSuperoxide DismutaseAngiotensin IINADPH OxidasesBiological TransportCell BiologyRespiratory burstMitochondriaPeroxidesEnzyme ActivationCrosstalk (biology)Oxidative StressMitochondrial permeability transition poreBiochemistrychemistrybiology.proteincardiovascular systemGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidation-ReductionOxidative stressCyclophilin D
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Prognostic value of blood pressure in patients with high vascular risk in the Ongoing Telmisartan Alone and in combination with Ramipril Global Endpo…

2009

Hypertension guidelines advise aggressive blood pressure (BP) lowering in patients with diabetes or high cardiovascular risk, but supporting evidence is limited. We analysed the impact of BP on cardiovascular events in well treated high-risk patients enrolled in a large clinical trial (Ongoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial).Twenty-five thousand five hundred and eighty-eight patients with atherosclerotic disease or diabetes with organ damage, tolerant to angiotensin-converting enzyme inhibitors, were randomized to ramipril, telmisartan or both. We related the primary composite outcome and its components to: baseline SBP; SBP changes from baseline to…

RamiprilMalemedicine.medical_specialtyPhysiologyAngiotensin-Converting Enzyme InhibitorsBlood PressureBenzoateslaw.inventionRandomized controlled trialDouble-Blind MethodRamiprillawInternal medicineInternal MedicinemedicineHumansTelmisartanRisk factorAntihypertensive AgentsAgedVascular diseasebusiness.industryMiddle Agedmedicine.diseasePrognosisAngiotensin IISurgeryClinical trialBlood pressureTreatment OutcomeHypertensionCardiologyBenzimidazolesFemaleTelmisartanCardiology and Cardiovascular Medicinebusinessmedicine.drugJournal of hypertension
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Antihypertensive and cardiovascular effects of combined blockade of renin-angiotensin system with ACE inhibitor and angiotensin II type 1 receptor bl…

2006

BACKGROUND.: In this study the effects of 24 weeks losartan and ramipril treatment, both alone and in combination, on blood pressure and left ventricular mass (LVM) and function, have been evaluated in hypertensives. METHODS.: 57 hypertensives with stage 1 and 2 essential hypertension were included. After 4 weeks run in, a randomized double-blind, 3 arm, double dummy, independent trial was used. All patients were randomly allocated to 3 treatment arms consisting of losartan (50 mg/daily), ramipril (5 mg/daily), and combined (losartan 50 mg/ramipril 5 mg/daily) for 24 weeks. LVM, LVM/h(2.7) and other echocardiographic measurements, BUN, creatinine and clearance and potassium were determined …

Ramiprillcsh:Diseases of the circulatory (Cardiovascular) systemmedicine.medical_specialtyLeft ventricular geometry and functionAngiotensin II receptor blockersLeft ventricular hypertrophyEssential hypertensionArticlechemistry.chemical_compoundInternal medicinemedicineAce-inhibitors Angiotensin II receptor blockers Left ventricular geometry and functioncardiovascular diseasesAce-inhibitorsCreatininebusiness.industrymedicine.diseaseAngiotensin IILosartanBlood pressurechemistrylcsh:RC666-701ACE inhibitorCardiologyCardiology and Cardiovascular Medicinebusinessmedicine.drugHeart International
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