Arterial hypertension plays an important role in the progress of cardiovascular disorders. The pressure level is directly addicted to the total peripheral resistance, which is determined by the diameter of the small arterioles. The endothelium controls vascular tone by different pathways. But not only releasing nitric oxide (NO) and prostacyclin dilate the underlying smooth muscle cells. Also the hyperpolarization of the endothelium causes a hyperpolarization and relaxation. This endothelium-derived hyperpolarizing factor (EDHF) is not completely understood but the small-conductance calcium-activated channels KCa3.1 und KCa2.3 play an important role in the hyperpolarisation of the endothelium. Sankaranarayanan et al. demonstrate in electrophysiological patch-clamp studies that the Riluzole derivative SKA-31 is able to open KCa3.1 channels with an EC50 of 250 nM and the KCa2.3 channel with an EC50 in the low micromolar range. This dissertation has the aim to investigate the pharmacological potency of SKA-31 in matters of amplifying the EDHF-answer. The studies were accomplished with Arteriae carotis communis and a pressure myographe system under physiological conditions. The needed KCa3.1 wildtype and knockout mice were reared and genotyped. SKA-31 potentiated the endothelium-derived-hyperpolarizing-factor-mediated-dilation with an EC50 of 93 nmol/L. It also reduced the need concentration of acetylcholine, but the contraction behaviour was not affected by SKA-31. The sole injection showed no dilation effect, so it seems possible that SKA-31 inhibits the closing of KCa3.1. Parllel organized experiments showed that SKA-31 is able to lower blood pressure in normtensiv and hypertensive mice and had no effect to the heart rate or toxic attributes. In summary SKA-31 shows the potential to be a new drug in the treatment of hypertension.