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Related Experiment Videos

Lipopolysaccharides decrease angiotensin converting enzyme activity expressed by cultured human endothelial cells.

K Watanabe1, G Lam, R S Keresztes

  • 1Department of Medicine, Cornell University Medical College, New York, New York 10021.

Journal of Cellular Physiology
|February 1, 1992
PubMed
Summary
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Lipopolysaccharide (LPS) significantly reduces angiotensin converting enzyme (ACE) activity on endothelial cells, potentially contributing to septic shock by lowering blood pressure regulation.

Area of Science:

  • Endothelial cell biology
  • Immunology
  • Cardiovascular physiology

Background:

  • Angiotensin converting enzyme (ACE) regulates blood pressure by converting angiotensin I to angiotensin II and metabolizing bradykinin.
  • ACE activity is diminished in vivo during sepsis.
  • Lipopolysaccharide (LPS) is a key component of Gram-negative bacteria, implicated in sepsis pathogenesis.

Purpose of the Study:

  • To investigate the effect of lipopolysaccharide (LPS) on angiotensin converting enzyme (ACE) activity in human umbilical vein endothelial cells (HUVEC).
  • To determine the dose- and time-dependency of LPS-induced ACE suppression.
  • To explore the mechanism underlying LPS-mediated inhibition of endothelial ACE activity.

Main Methods:

  • Human umbilical vein endothelial cells (HUVEC) were cultured with varying concentrations and durations of LPS exposure.

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  • ACE activity was measured in intact HUVEC monolayers.
  • Cellular cytotoxicity and kinetic parameters (Vmax, Km) of ACE were assessed.

    • Main Results:

    • LPS markedly suppressed HUVEC ACE activity in a time-dependent manner, with significant inhibition observed after 24, 48, and 72 hours.
    • The suppression was dose-dependent, with an IC50 of 15 ng/ml at 24 hours, and detectable at LPS concentrations as low as 1 ng/ml.
    • LPS reduced ACE Vmax without altering Km, suggesting a decrease in the amount of ACE on the cell membrane, and the effect was partially reversible.

    Conclusions:

    • Lipopolysaccharide (LPS) directly suppresses endothelial cell ACE activity.
    • This LPS-induced reduction in ACE may contribute to the decreased angiotensin II production and altered bradykinin metabolism observed in sepsis.
    • The findings suggest a role for LPS in the pathogenesis of septic shock via modulation of endothelial ACE function.