The occurrence of left ventricular hypertrophy (LVH) has been shown to be a powerful determinant of cardiovascular morbidity and mortality in hypertensive patients [1]. As the blood pressure level only partly explains the variation in left ventricular mass (LVM) and medical intervention by means of antihypertensive treatment only induces a partial regression of the LVH [2], further investigations of the mechanisms underlying the development of LVH are motivated. A raised total peripheral vascular resistance (TPR), giving rise to an increased afterload of the left ventricle, is generally accepted as one major pathogenetic mechanism that promotes the development of LVH. Since the observed impairment of endothelium-dependent vasodilation (EDV) found in hypertensive patients [3–10] might contribute to an increase in TPR, such an abnormality could be of pathogenetic importance for the development of LVH. However, the studies addressing this issue so far have yielded divergent results when EDV was estimated in the forearm circulation. Both an association between an impaired EDV and LVH [11], as well as no association [12] between these cardiovascular characteristics were reported. The primary aim of the present study was therefore to further investigate the relation between EDV and LVM in untreated hypertensive patients. This was carried out by means of forearm blood ow (FBF) measurements with venous occlusion plethysmography during local intraarterial infusions of methacholine (MCh, evaluating EDV) and sodium nitroprusside (SNP, evaluating endothelium-independent vasodilation, EIDV), echocardiography was used to determine LVM. A secondary aim of the study was to investigate if such a relationship also exists in a sample of treated hypertensive patients.