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See related article, pp 337–344In the current issue of Hypertension , Virdis et al1 report an elegant series of experiments on isolated small arteries harvested from normotensive and essential hypertensive humans. They conclude that, in the blood vessels of their hypertensive subjects, cyclooxygenase-2 (COX2) represents a major source of reactive oxygen species (ROS), in particular superoxide anions, which in turn reduces the bioavailability of NO, thus curtailing endothelium-dependent relaxations to acetylcholine. They feel that these observations provide the major explanation for the endothelial dysfunction characteristic of human essential hypertension. The data reported1 are convincing, despite the small size of the studied populations, which indirectly reinforces the importance of the mechanism revealed. As such, these findings seem to provide the finishing touch to a translational picture drafted more than a quarter of a century ago in the aorta of the essential spontaneously hypertensive rat (SHR)2 and thereafter outlined in the human forearm.3One can always find imperfections in any study (except one’s own!). A common temptation is to use only 1 dose of a pharmacological agent and to believe in its selectivity. For example, in the study by Virdis et al,1 only a minor role for NAD(P)H oxidase (by most believed to be the main generator of superoxide anions in the vascular wall) is inferred from the modest effect of single concentrations of apocynin and diphenylene iodinium, presented as selective inhibitors of this enzyme. However, the latter agent interferes with several other flavoenzyme oxidoreductases, and the former is regarded (at least in Frankfurt) as a nonselective antioxidant that should yield effects comparable with those of ascorbic acid. Similarly, …

One or Two, Does it Matter as Long as the Arterial Wall Is Coxygenated?