Essential arterial hypertension (EH) is an important risk factor for atherosclerosis. There is growing evidence that endothelial dysfunction is the earliest event in atherogenesis and also precedes morphological changes of the arterial wall in hypertensive patients.1 One of the most widely recognised methods of determining the endothelial function is the dilation capability of arteries. Risk factors of atherosclerosis, including EH, probably decrease the production and increase the consumption of nitric oxide which plays a central role in the vasodilation.

Studies where venous occlusion plethysmography was used for measurement of changes in the blood flow demonstrated that patients with EH showed impaired endothelium dependent vasodilation of peripheral resistance arteries. On the other hand, there is only little evidence, albeit controversial, of the dilation capability of systemic conduit arteries in EH patients.2-4

The aim of the present study was to evaluate non-invasively whether flow-mediated dilation (FMD) of the brachial artery is also impaired, in spite of treatment in patients with EH, and to find whether these abnormalities precede clinical manifestations of elevated blood pressure and can therefore be detected in the normotensive offspring of subjects with EH (hypertensive familial trait (FT)).

The study encompassed four groups involving a total of 172 subjects. In the first group there were 46 patients (35 men and 11 women, mean age 49 years) with the EH documented for at least two years. Only hypertonics with well documented elevated blood pressure (⩾ 145/95 mm Hg in a sitting position in at least three different measurements before starting treatment) were included. The hypertensive subjects took their medication (either long acting calcium channel antagonists or angiotensin converting enzyme (ACE) inhibitors) 6–8 hours before haemodynamic measurements were performed. The second group of 44 healthy normotensive subjects (32 men and 12 women), matched with the patients in age and sex, served as …