“…noradrenalin, rennin-angiotensin-aldosterone and arginine vasopressin) and vasodilators (i.e. NO, glucagon, vasoactive peptide and substance P) have been measured in the setting of portal hypertension [186][187][188]. In short, investigators have hypothesised that an imbalance of vasoactive substances could reach the pulmonary circulation in abnormally high concentrations due to portosystemic shunts or defective hepatic metabolism, causing the pathological pulmonary vascular lesions seen in PPHTN [6,153].…”