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Related Experiment Videos

Glomerular dysfunction induced by polymorphonuclear leukocyte-derived reactive oxygen species.

T Yoshioka1, I Ichikawa

  • 1Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2584.

The American Journal of Physiology
|July 1, 1989
PubMed
Summary

Reactive oxygen species from activated polymorphonuclear leukocytes significantly reduce glomerular filtration rate. This effect on kidney microcirculation is mediated by ROS and can be prevented by antioxidants or PMN depletion.

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Area of Science:

  • Nephrology
  • Physiology
  • Immunology

Background:

  • Polymorphonuclear leukocytes (PMN) are key immune cells involved in inflammation.
  • Reactive oxygen species (ROS) are byproducts of cellular metabolism with signaling roles.
  • The specific impact of PMN-derived ROS on glomerular microcirculation requires further elucidation.

Purpose of the Study:

  • To investigate the role of reactive oxygen species (ROS) generated by polymorphonuclear leukocytes (PMN) in modulating glomerular microcirculation.
  • To determine the effect of PMN activation on glomerular filtration rate (GFR) and intrarenal hemodynamics.

Main Methods:

  • Munich-Wistar rats were used to study glomerular microcirculation.
  • Phorbol myristate acetate (PMA) was infused unilaterally into the renal artery to activate local PMN.

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  • Micropuncture studies were conducted 18 hours post-infusion to assess glomerular PMN accumulation, GFR, and microcirculatory dynamics.

    • Main Results:

    • PMA infusion led to significant glomerular PMN accumulation in the treated kidney.
    • A marked reduction in whole kidney and single-nephron GFR was observed in PMA-treated kidneys.
    • Pretreatment with catalase (a hydrogen peroxide scavenger) or PMN depletion prevented the GFR reduction.

    Conclusions:

    • ROS derived from activated PMN play a critical role in reducing glomerular filtration rate.
    • Activated PMN significantly impair glomerular microcirculation, leading to decreased GFR and altered intrarenal hemodynamics.
    • Targeting PMN-derived ROS may offer a therapeutic strategy for kidney injury involving inflammation.