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Endothelial Dysfunction in Resistance Arteries of Hypertensive Humans: Old and New Conspirators

Virdis, Agostino MD; Taddei, Stefano MD

Journal of Cardiovascular Pharmacology: June 2016 - Volume 67 - Issue 6 - p 451–457
doi: 10.1097/FJC.0000000000000362
Invited Review Article
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Abstract: A large body of homogeneous reports documented that endothelial dysfunction, which characterizes human essential hypertension is largely dependent on an impaired endothelial nitric oxide availability and an increased production of endothelium-derived contracting factors. These factors include endothelin, prostanoids, and reactive oxygen species (ROS). In particular, it was evidenced that acute intraarterial administration of indomethacin, a nonselective cyclooxygenase (COX)-inhibitor, and ascorbic acid, an antioxidant, normalized the blunted endothelial dysfunction by restoring nitric oxide availability at the level of peripheral microcirculation, thus demonstrating that COX-derived endothelium-derived contracting factors are one of the major sources of ROS. Recent studies put in evidence new lights on the mechanisms involved in endothelial dysfunction in human hypertension, identified as “new conspirators.” In particular, functional and immunohistochemical experiments with selective COX inhibitors identified the isoform COX-2 as the main source of intravascular ROS generation in isolated small vessels from essential hypertensive patients. In addition, important vascular protective properties by human ghrelin have been demonstrated in human hypertension, in terms that its systemic reduction is involved in the pathophysiology of endothelial dysfunction, while a normalization of its levels may restore vascular homeostasis.

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Reprints: Stefano Taddei, MD, Department of Clinical and Experimental Medicine, University of Pisa, Via Roma 67, 56100 Pisa, Italy (e-mail: stefano.taddei@med.unipi.it).

The authors report no conflicts of interest.

Received September 23, 2015

Accepted January 05, 2016

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