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Endothelium-dependent contractions: when a good guy turns bad!

Paul M Vanhoutte1, Eva H C Tang

  • 1Department of Pharmacology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong SAR, China. vanhoutt@hkucc.hku.hk

The Journal of Physiology
|September 27, 2008
PubMed

Insights

Endothelial cells generate vasoconstrictor prostanoids (EDCF) that contract vascular smooth muscle, primarily via the COX-1 enzyme. Nitric oxide (NO) inhibits EDCF production, impacting conditions like hypertension.

Area of Science:

  • Vascular biology
  • Endothelial function
  • Prostanoid signaling

Background:

  • Endothelial cells regulate vascular tone by producing endothelium-dependent contracting factors (EDCF).
  • The cyclooxygenase-1 (COX-1) isoform is key in EDCF generation, requiring intracellular calcium increase.
  • Nitric oxide (NO) and endothelium-dependent hyperpolarizing factor (EDHF) can inhibit EDCF production.

Purpose of the Study:

  • To elucidate the mechanisms and signaling pathways of endothelium-dependent contractions.
  • To identify the specific prostanoids and receptors involved in EDCF-mediated vasoconstriction.
  • To understand the role of EDCF in endothelial dysfunction associated with aging and hypertension.

Main Methods:

  • Investigated the role of endothelial COX-1 in EDCF production.
  • Examined the influence of intracellular Ca(2+) on EDCF generation.
  • Assessed the inhibitory effects of NO and EDHF on EDCF.
  • Identified prostanoids (PGH(2), prostacyclin) and TP receptor activation.
  • Studied the impact of free radicals on EDCF action.

Main Results:

  • Endothelial COX-1 is dominant in generating EDCF.
  • EDCF production is calcium-dependent.
  • Nitric oxide (NO) acutely and chronically inhibits EDCF.
  • Endoperoxides (PGH(2)) and prostacyclin acting on TP receptors mediate contractions.
  • Oxygen-derived free radicals can enhance EDCF production/action.

Conclusions:

  • EDCF, mediated by COX-1, PGH(2), prostacyclin, and TP receptors, contributes to vascular smooth muscle contraction.
  • NO and EDHF act as endogenous inhibitors of EDCF.
  • Impaired EDCF regulation is linked to endothelial dysfunction in aging, obesity, hypertension, and diabetes.

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