As far as patients suffering from hepatic fibrosis are concerned, a transient increase in blood pressure may be noticed, in the first stage, related to stimulation of the sympathetic nervous system, release of endothelin 1 (ET-1), neuropeptide Y, and stimulation of the renin–angiotensin–aldosterone system (RAA), which leads to hyperaldosteronism, the retention of sodium and water and an increased level of vasopressin, which contributes to the increase in blood pressure without significant pressure increase in the portal vein and an increase in ascites. Here, EDN1 is linked to hyperaldosteronism.