Participation of peripheral polymorphonuclear leukocytes in the oxidative stress and inflammation in patients with essential hypertension

Batya Kristal, Revital Shurtz-Swirski, Judith Chezar, Joseph Manaster, Rivka Levy, Galina Shapiro, Irith Weissman, Shaul M. Shasha, Shifra Sela

Research output: Contribution to journalArticlepeer-review

124 Scopus citations


Oxidative stress and inflammation have recently been linked to endothelial damage in essential hypertension (EH). Activated peripheral polymorphonuclear leukocytes (PMN) damage surrounding tissue by releasing reactive oxygen species (ROS) and proteolytic enzymes before self-necrosis. PMN necrosis further exacerbates inflammation and promotes chemotaxis and PMN recruitment. The number and properties of PMN from untreated EH patients is the focus of the present study. Oxidative stress was assessed by measuring the rate of superoxide anion release from separated, phorbol ester-stimulated PMN and the redox state of plasma glutathione. Inflammation was estimated indirectly by determining PMN number and their in vitro survival. PMN from EH patients (n = 37) released superoxide anion faster (P < .0001) than those of normotensives (NC, n = 37), 17.7 ± 1.14 v 9.54 ± 0.51 nmol/10 min/106 cells. The redox state of glutathione was twofold higher in EH plasma (P < .02) indicating systemic oxidative stress. PMN survival in vitro correlates linearly with the rate of superoxide release (r2 = 0.60, P < .02) and PMN count of EH patients, although in the normal range, were significantly higher (P < .0001), indicating necrosis and recruitment. Hypertensive plasma significantly reduced NC PMN viability, whereas normal plasma significantly increased EH PMN viability. What our studies show is that EH is accompanied by a primed state PMN that does not correlate with the levels of blood pressure. PMN priming in EH patients reflects an in vivo exposure to a constant stimulus ending in oxidative stress, increased self-necrosis, and cell recruitment. Oxidative stress and inflammation will result in endothelial damage and atherosclerosis in the long run.

Original languageEnglish
Pages (from-to)921-928
Number of pages8
JournalAmerican Journal of Hypertension
Issue number8 I
StatePublished - Aug 1998
Externally publishedYes


  • Hypertension
  • Necrosis
  • Oxidized glutathione
  • Polymorphonuclear leukocytes
  • Superoxide release


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