The first abnormality leading to sodium and water retention in cirrhosis is the renal tubular defect that is related to deteriorating liver function and hyperaldosteronism. With progression of liver disease and portal hypertension, renal blood flow declines because of the hepatorenal reflex, and is then maintained by the vasoactive hormonal systems. With increasing peripheral vasodilatation, intrarenal factors for maintenance of renal perfusion cause intense cortical vasoconstriction. The systemic vasoactive factors are predominantly compensatory; any attempts to counteract their action risk circulatory collapse. Future studies should be directed at intrarenal factors. The ideal drug for the treatment of portal hypertension would reduce portal pressure, increase renal blood flow, and produce insignificant changes in arterial pressure.