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G-proteins and endothelial responses.

N A Flavahan1, P M Vanhoutte

  • 1Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Md.

Blood Vessels
|January 1, 1990
PubMed
Summary

Certain endothelial relaxations involve G-proteins sensitive to pertussis toxin. Regenerating endothelial cells show impaired G-protein function, potentially increasing vascular disease risk.

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Area of Science:

  • Cardiovascular Physiology
  • Molecular Pharmacology
  • Endothelial Cell Biology

Background:

  • G-proteins are crucial for signal transduction, linking membrane receptors to intracellular effectors.
  • Pertussis toxin inhibits G-protein function by ADP-ribosylation, affecting cellular signaling pathways.

Purpose of the Study:

  • To investigate the role of pertussis toxin-sensitive G-proteins in mediating endothelium-dependent relaxations in porcine coronary arteries.
  • To examine the functional status of these G-protein pathways in regenerating endothelial cells.

Main Methods:

  • Utilized pertussis toxin to assess the involvement of G-proteins in endothelial responses.
  • Studied porcine coronary arteries with intact and regenerated endothelium.
  • Measured endothelium-dependent relaxations induced by various receptor agonists and stimuli.

Main Results:

  • Pertussis toxin inhibited relaxations mediated by alpha-2-adrenergic and serotonergic stimulation, as well as by platelets and thrombin.
  • Nitric oxide-mediated relaxations and others (bradykinin, ADP, A23187) were unaffected by the toxin.
  • In arteries with regenerated endothelium, pertussis toxin-sensitive relaxations were reduced and unresponsive to the toxin.

Conclusions:

  • Endothelium-dependent relaxations in coronary arteries are partly mediated by pertussis toxin-sensitive G-proteins, likely Gi-proteins.
  • Regenerating endothelial cells exhibit a selective impairment in G-protein-dependent signaling for EDRF release.
  • This impairment may contribute to vasospasm and vascular disease initiation.

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