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

Cardiovascular Physiology

DOI: 10.1007/s00424-010-0786-4

Cite this article as:
Tang, E.H.C. & Vanhoutte, P.M. Pflugers Arch - Eur J Physiol (2010) 459: 995. doi:10.1007/s00424-010-0786-4


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 

Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  1. 1.Division of Cardiovascular Medicine, Brigham and Women’s HospitalHarvard Medical SchoolBostonUSA
  2. 2.Department Pharmacology and Pharmacy, Li Ka Shing Faculty of MedicineUniversity of Hong KongHong KongChina
  3. 3.Department BIN Fusion TechnologyChonbuk National UniversityJeonjuKorea

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