Key result
Polymorphonuclear leukocytes contribute to vascular damage in arterial hypertension through the release of proinflammatory factors, reactive oxygen species, and overexpression of adhesion molecules.
This review highlights the pathophysiological mechanisms by which polymorphonuclear leukocytes mediate vascular damage and organ injury in arterial hypertension.
Answers are grounded in this paper and cite their sources.
Supports leukocyte-targeted research in hypertension; leaves open whether modulation improves clinical outcomes.
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.
No takes yet. Share an insight, caveat, or question.
Hopps et al. (2009) conducted a review in Arterial hypertension. Polymorphonuclear leukocytes (PMNs) activation was evaluated. Polymorphonuclear leukocytes contribute to vascular damage in arterial hypertension through the release of proinflammatory factors, reactive oxygen species, and overexpression of adhesion molecules.
Synapse has enriched 10 related papers. Consider them for comparative context: