Activation of Vascular Smooth Muscle K+Channels by Endothelium-Derived Factors

  • Michel Félétou
  • Paul M. Vanhoutte

Abstract

Endothelial cells synthesize and release vasoactive mediators in response to various neurohumoral substances (e.g., acetylcholine, ATP, bradykinin, thrombin) and physical stimuli (e.g., shear stress exerted by the flowing blood) (Furchgott and Vanhoutte, 1989). Nitric oxide (NO) produced by the L-arginine—NO synthase pathway and prostacyclin produced from arachidonic acid by cyclooxygenase have been identified as potent endothelium-derived vasodilators (Moncada et al., 1976; Moncada and Vane, 1979; Furchgott and Zawadzki, 1980; Palmer et al., 1987, Palmer 1988). However, not all endothelium-dependent relaxations can be fully explained by the release of either NO or prostacyclin. Indeed, another unidentified substance(s) which hyperpolarizes the underlying vascular smooth muscle cells, termed endothelium-derived hyperpolarizing factor (EDHF), may contribute to endothelium-dependent relaxations (Furchgott and Vanhoutte, 1989; Komori and Vanhoutte, 1990; Félétou and Vanhoutte, 1996a; Mombouli and Vanhoutte, 1997).

Keywords

Carbon Monoxide Barium Prostaglandin Cardiol Thrombin 

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References

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Copyright information

© Springer Science+Business Media New York 2001

Authors and Affiliations

  • Michel Félétou
    • 1
  • Paul M. Vanhoutte
    • 2
  1. 1.Département de DiabétologieInstitut de Recherches ServierSuresnesFrance
  2. 2.Institut de Recherches Internationales ServierCourbevoieFrance

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