 In subjects with impaired glucose tolerance IGT, insulin resistance and dysfunction of pancreatic beta-cells in variable contribution have already established increased postprandial hyperglycemia with a consecutively increased cardiovascular risk 4, 5. In addition they have a considerable risk for future development of manifest type-II diabetes in the range of 3-6 within a year 6, 7. In such patients prevention of diabetes may also result in cardiovascular prevention. As subjects with IGT often exhibit a more or less pronounced metabolic syndrome, hypertension is a frequently found comorbidity and vice versa IGT is frequent in hypertensive patients suggesting a possible common soil of the two diseases 8. 