Background: Portal Hypertension is considered an abnormal elevation of pressure in the veins that drain blood from the visceral organs (e.g., the spleen) to the liver. This occurs due to elevated resistance to blood flow in the portal circulation with the development of collateral circulation to carry portal blood. Reducing portal pressure and avoiding portal hypertension-related problems are the goals of the pharmacological management of portal hypertension. Portal blood flow and hepatic vascular resistance determine portal pressure. We aimed to present an insight into the pharmacological management of portal hypertension.

Conclusion: The main goals of current medications in portal hypertension. are to either reduce the formation of collateral circulation, hyperdynamic circulation, vascular hyperplasia, renin-angiotensin-aldosterone system (RAAS) activation, or to inhibit angiogenesis and fibrosis in the liver to decrease intravascular resistance. Portal hypertension causes splanchnic and systemic arterial vasodilation, which in turn activates the neurohumoral (increase in sympathetic activity and activation of the RAAS) and vasoconstrictive systems; this leads to increased cardiac output, increased blood volume, and sodium and water retention. Activation of the RAAS raises portal pressure, according to multiple investigations in cirrhotic animals and people