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RESEARCH PRODUCT
Pathophysiology of polymorphonuclear leukocyte in arterial hypertension
Gregorio CaimiEugenia HoppsRosalia Lo Prestisubject
medicine.medical_specialtyEndotheliumNeutrophilsPhysiologyPolymorphonuclear leukocyte Hypertension oxidative stress adhesion moleculesmedicine.disease_causeProinflammatory cytokineSuperoxide dismutaseLipid peroxidationLeukocyte Countchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansLeukocyte Rollingchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxide Dismutasebusiness.industryCell adhesion moleculeNADPH OxidasesHematologymedicine.anatomical_structureEndocrinologychemistryCD18 AntigensHypertensionImmunologybiology.proteinLipid PeroxidationCardiology and Cardiovascular MedicinebusinessOxidative stressdescription
This review shows how polymorphonuclear leukocytes (PMNs) play a pivotal role in the development of the organ injury that is associated with arterial hypertension. Elevated white blood cell count and higher levels of PMNs activation are risk factors for arterial hypertension and cardiovascular disease. Spontaneously activated PMNs release proinflammatory factors and reactive oxygen species, which have negative effects on vascular tone and on their adhesion to the endothelium. The oxidative stress in hypertensive PMNs is revealed by increased NADPH-oxidase production and lipid peroxidation and by decreased cytosolic and mitochondrial superoxide dismutase concentrations. The overexpression of adhesion molecules, such as beta2-integrin, promotes PMNs rolling and leukocyte-endothelium interactions too. All these events underline how polymorphonuclear leukocytes may contribute to the vascular damage accompanying arterial hypertension.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2009-03-12 | Clinical Hemorheology and Microcirculation |