This review highlights that while endothelial dysfunction is linked to hypertension, current antihypertensive therapies are largely unable to reverse it, and better parameters for assessing endothelial dysfunction are needed.
Endothelial dysfunction testing should not guide antihypertensive choices; leaves open targeted reversal strategies and better assessment parameters.
Hypertension is an important risk factor for the development of atherosclerosis and endothelial dysfunction may be a key mechanism. The nitric oxide mediated vasodilator function of the endothelium has been widely studied as a test of endothelial integrity in patients with hypertension and impaired basal and muscarinic agonist stimulated components of nitric oxide mediated vascular tone have been found in coronary, forearm and cutaneous resistance vessels and in coronary and forearm conduit vessels. The underlying abnormalities of these changes are unknown but it is likely to be a secondary phenomenon due to increased blood pressure. However, endothelial dysfunction as assessed by response to muscarinic agonists does not occur in all patients and antihypertensive therapy so far has been mostly unable to reverse it. Although widely used the response to acetylcholine has some shortcomings and it remains to be established what parameter best reflects endothelial dysfunction. The relationship of such abnormalities to the present or future atherosclerosis needs to be defined.
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Wolfgang Kiowski (1999) studied this question.
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