In early cirrhosis, increased portal pressure is primarily caused by enhanced hepatic vascular resistance. This resistance stems from endothelial dysfunction, which leads to diminished nitric oxide production and subsequent sinusoidal vasoconstriction. The structural changes are minimal initially, so dynamic factors like endothelial injury dominate the rise in portal pressure. This mechanism explains why portal hypertension can develop before significant fibrosis or hepatocyte loss occurs. Addressing endothelial dysfunction is therefore crucial in managing early portal hypertension.

Reference: Harrison's Principles of Internal Medicine, Jameson et al., 20th Edition.