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Endothelial dysfunction in hypertension

P M Vanhoutte1

  • 1Institut de Recherches Internationales Servier (IRIS), Courbevoie, France.

Journal of Hypertension. Supplement : Official Journal of the International Society of Hypertension
|December 1, 1996
PubMed
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Endothelial cells in hypertension release fewer relaxing factors like nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), contributing to vascular dysfunction. This dysfunction is a consequence, not a cause, of hypertension.

Area of Science:

  • Vascular Biology
  • Endocrinology
  • Hypertension Research

Background:

  • The endothelium regulates vascular tone via releasing relaxing and contracting factors.
  • Key relaxing factors include prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF).
  • Contracting factors include endoperoxides, thromboxane A2, superoxide anions, and endothelin.

Purpose of the Study:

  • To elucidate the role of abnormal endothelial factor release in hypertension-related vascular abnormalities.
  • To summarize the contribution of endothelial dysfunction to the pathophysiology of hypertension.

Main Methods:

  • Review and synthesis of existing literature on endothelial function in hypertension.
  • Analysis of the balance between endothelium-derived relaxing and contracting factors.

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Main Results:

  • Hypertension is characterized by reduced endothelium-dependent relaxations due to decreased NO and EDHF production or action.
  • Essential hypertension involves reduced relaxations and increased vasoconstrictor prostanoids (endoperoxides, thromboxane A2).
  • Endothelial dysfunction in hypertension appears to be a consequence, not a primary cause.

Conclusions:

  • Enhanced release of NO and EDHF contributes to the therapeutic benefits of angiotensin-converting enzyme inhibitors.
  • Restoring endothelial function is a potential therapeutic strategy for hypertension.