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Published on: January 4, 2018
Pathophysiology of polymorphonuclear leukocyte in arterial hypertension
Eugenia Hopps1, Rosalia Lo Presti, Gregorio Caimi
1Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche, Cattedra di Semeiotica e Metodologia Medica, Università di Palermo, Palermo, Italy.
Abstract:
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.
Insights
Polymorphonuclear leukocytes (PMNs) contribute to organ injury in arterial hypertension. Activated PMNs increase inflammation and oxidative stress, damaging blood vessels and worsening cardiovascular disease risk.
Area of Science:
- Cardiovascular Science
- Immunology
- Pathophysiology
Background:
- Arterial hypertension is linked to organ injury.
- Elevated white blood cell counts and activated polymorphonuclear leukocytes (PMNs) are risk factors for hypertension and cardiovascular disease.
Purpose of the Study:
- To review the role of PMNs in arterial hypertension-associated organ injury.
- To elucidate the mechanisms by which PMNs contribute to vascular damage in hypertension.
Main Methods:
- Literature review focusing on PMN activation and function in hypertension.
- Analysis of molecular and cellular events involving PMNs and vascular endothelium.
Main Results:
- Activated PMNs release inflammatory factors and reactive oxygen species, impairing vascular tone and promoting endothelial adhesion.
- Hypertensive PMNs exhibit increased oxidative stress, evidenced by higher NADPH-oxidase and lipid peroxidation, and lower superoxide dismutase levels.
- Overexpression of adhesion molecules like beta2-integrin on PMNs enhances leukocyte-endothelium interactions.
Conclusions:
- PMNs are key players in the vascular damage associated with arterial hypertension.
- PMN activation contributes to hypertension-related organ injury through inflammatory and oxidative mechanisms.
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