Dysregulation of vascular contractile signaling in liver cirrhosis: Rho-kinase as molecular basis for portal hypertension

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Cirrhosis of the liver is associated with the development of portal hypertension. The increase in portal pressure results from hernodynamic and vascular abnormalities ccurlng during cirrhosis (1-6). These are an increased splanchnic flaw due to persistent mesenteric vasodilation, and an impaired portal outftow which is related to an increased intrahepatic resistance [44). Importantly, portal hypertension is responsible for the most carnmsln and most Ilfe-threatening complications resulling from cirrhosis (1,3,10). Thus, as a result of portal hypertension, colbteral blood vessels are being formed, which bypaas the liver, so that the Mood flows from the pori~il vein directly into systemic and peripheral vessels (4,11). In human cirrhosis, this leads to the formation of gastro-esophageal varices. Subsequent variceal bleeding is by far the most common reason of death in patients with cirrhosis (4,11-15). Therefore, the pa pathophysiological mechanisms underlying portal hypertension are of major interest.

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