Cardiovascular Physiology

Pflügers Archiv - European Journal of Physiology

, Volume 459, Issue 6, pp 995-1004

First online:

Endothelial dysfunction: a strategic target in the treatment of hypertension?

  • Eva H. C. TangAffiliated withDivision of Cardiovascular Medicine, Brigham and Women’s Hospital, Harvard Medical School Email author 
  • , Paul M. VanhoutteAffiliated withDepartment Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, University of Hong KongDepartment BIN Fusion Technology, Chonbuk National University

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Endothelial dysfunction is a common feature of hypertension, and it results from the imbalanced release of endothelium-derived relaxing factors (EDRFs; in particular, nitric oxide) and endothelium-derived contracting factors (EDCFs; angiotensin II, endothelins, uridine adenosine tetraphosphate, and cyclooxygenase-derived EDCFs). Thus, drugs that increase EDRFs (using direct nitric oxide releasing compounds, tetrahydrobiopterin, or l-arginine supplementation) or decrease EDCF release or actions (using cyclooxygenase inhibitor or thromboxane A2/prostanoid receptor antagonists) would prevent the dysfunction. Many conventional antihypertensive drugs, including angiotensin-converting enzyme inhibitors, calcium channel blockers, and third-generation β-blockers, possess the ability to reverse endothelial dysfunction. Their use is attractive, as they can address arterial blood pressure and vascular tone simultaneously. The severity of endothelial dysfunction correlates with the development of coronary artery disease and predicts future cardiovascular events. Thus, endothelial dysfunction needs to be considered as a strategic target in the treatment of hypertension.


Endothelium Prostaglandin Contraction Free radical Hypertensive rats