Introduction: Arterial hypertension is the leading risk factor for mortality worldwide. The increasing number of studies support the hypothesis that endothelial dysfunction due to reduced availability of nitric oxide plays a key role in initiation, development and progression of essential hypertension. The aim of our study was to determine whether the ingestion of the food supplement L-arginine actually improves endothelial function, which could be beneficial in the treatment of essential hypertension. Methods: 30 normotensive healthy men, aged 20-30 years, were divided into two groups according to the family history of hypertension (FN – healthy, not genetically predisposed, FH – normotensive subjects with family history of hypertension). We measured ECG, heart rate, systolic and diastolic blood pressure, cardiac output, stroke volume, total peripheral resistance (Task Force Monitor) and laser Doppler (LD) flux in the microvessels of the skin of the forearm, at rest before and after administration of 0.9 g L-arginine. Endothelium-dependent vasodilation was assessed by iontophoresis of acetylcholine and endothelium-independent vasodilation by iontophoresis of sodium nitroprusside. Values are expressed as mean ± SEM. The study was approved by the National Medical Ethics Committee; written informed consent was obtained from each subject. Results: After the ingestion of L-arginine the heart rate (FN 67.7 ± 4.3 vs. 62.7 ± 3.3; FH 63.2 ± 2.2 vs. 60.3 ± 2.0 beats/min) and the cardiac output (FN 7.07 ± 0.5 vs. 6.53 ± 0.4; FH 7.19 ± 0.3 vs. 6.38 ± 0.2 L/min) statistically significantly decreased in both groups (paired t-test, p<0.05), while arterial blood pressure did not change significantly. In contrast, stroke volume decreased (116.0 ± 6.5 vs. 108.2 ± 5.9 mL) and total peripheral resistance increased (868.9 ± 96 vs. 1114.4 ± 48 MPa s/m3) only in the group of subjets with family history of hypertension (paired t-test, p<0.05). We demonstrated that the ingestion of L-arginine in genetically predisposed normotensive subjects acutely improved endothelium-dependent vasodilation (68.8 ± 4.4 vs. 95.4 ± 9.3 PU) (Dunnett’s test, p < 0.05), which is consistent with the assumption that endothelial dysfunction is already present in these subjects. Conclusions: In genetically predisposed normotensive subjects in comparison to healthy subjects without predisposition, L-arginine increased nitric oxide production and improved endothelial function. That justifies L-arginine as a potential therapeutic agent for treatment of arterial hypertension.