Portal hypertension is characterized by an increased portal pressure gradient which is the difference in pressure between the portal vein and the inferior vena cava and becomes clinically significant when the portal pressure gradient increases to 10 mmHg or above. Portal hypertension is responsible for many of the manifestations of liver cirrhosis. These manifestations such as gastrointestinal bleeding as a result of ruptured gastroesophageal varices and portal hypertensive gastropathy, colopathy and ascites are documented. Hepatorenal syndrome and hypersplenism are the direct consequences of portal hypertension. Stellate cell activation is a key event in liver injury, and indicates the transition from a quiescent vitamin A-rich cell to a highly fibrogenic cell. Activation consists of three major phases: initiation, perpetuation and resolution. Initiation refers to early paracrine-mediated changes in gene expression and phenotype that render the cells responsive to other cytokines and stimuli while perpetuation results from the effects of these stimuli on maintaining the activated phenotype and generating fibrosis. Portal hypertension secondary to hepatic fibrosis and cirrhosis has multisystem effects and multiple complications. The multisystem effects are hepatorenal, portopulmonary hypertension, hepatopulmonary syndrome, portal hypertensive colopathy and others. Once a patient develops any of such complications, he is considered to have decompensated disease with the high morbidity and mortality.