Therefore, we investigated the KCa3.1/KCa2.x channel activator SKA-31-induced systemic hemodynamic effects and the putative endothelium-dependent relaxation, including EDH-KCa2.3/KCa3.1 type, in isolated endothelium-intact sMAs in a rat genetic model of primary hypertension in order to check if it could be relevant for antihypertensive therapy/ beneficial in cardiovascular system in hypertension. The gene discussed is KCNN3; the disease is essential hypertension.