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Effects of activated polymorphonuclear leukocytes on vascular smooth muscle tone

J L Mehta1, D L Lawson, F A Nicolini

  • 1Department of Medicine, University of Florida College of Medicine, Gainesville.

Insights

Activated polymorphonuclear leukocytes (PMNLs) cause initial blood vessel contraction and subsequent relaxation. Superoxide radicals from PMNLs may cause contraction, while nitric oxide mediates relaxation.

Area of Science:

  • Cardiovascular Physiology
  • Inflammation Research
  • Vascular Biology

Background:

  • Polymorphonuclear leukocytes (PMNLs) are key immune cells involved in inflammation.
  • Unstimulated PMNLs release nitric oxide (NO), a vasodilator.
  • The effects of activated PMNLs on vascular tone are not fully understood.

Purpose of the Study:

  • To investigate the impact of activated PMNLs on vascular tone.
  • To elucidate the mechanisms underlying PMNL-induced vascular effects, including the roles of superoxide radicals and NO.

Main Methods:

  • Rat aortic rings were precontracted and exposed to unstimulated or ionophore-stimulated PMNLs.
  • Vascular responses were measured in the presence or absence of inhibitors and scavengers.
  • Superoxide radicals were generated using xanthine/xanthine oxidase (X + XO) to mimic PMNL-derived radicals.

Main Results:

  • Stimulated PMNLs induced initial contraction followed by significant vasodilation (90%).
  • Superoxide dismutase (SOD) abolished the initial contraction and attenuated relaxation, implicating superoxide radicals.
  • Deendothelialized or X + XO-treated rings showed enhanced relaxation to unstimulated PMNLs, supporting the role of endothelial damage and superoxide radicals.

Conclusions:

  • Activated PMNLs exert a biphasic effect on vascular tone: initial vasoconstriction followed by vasodilation.
  • Superoxide radical release by PMNLs contributes to initial vasoconstriction and potentially endothelial damage.
  • Nitric oxide release by PMNLs mediates the subsequent vasorelaxant effect.

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