Essential hypertension is characterized by impaired endothelial function. Data derived from normotensive subjects with a genetic predisposition to arterial hypertension suggest that endothelial dysfunction is a cause rather than a consequence of the condition. Given that, in normotensive offspring of hypertensive parents, impaired endothelium dependent vasodilation can be restored by supplementation of the nitric oxide (NO) precursor L-arginine, a defect in the L-arginine/NO pathway can be postulated. The investigators at the University of Erlangen-Nuremberg, hypothesize that impaired endothelial function in essential hypertension is associated with alterations in L-arginine metabolism and transport. This study will determine whether metabolism and transport of L-arginine are altered in patients with essential hypertension and whether these potential alterations can be targeted therapeutically.