Liver linked to deadly disease

Mechanisms causing a potentially deadly type of hypertension that results from liver damage have been identified by Don Rockey, a physician at the University of Texas Southwestern Medical Center, Dallas. Portal hypertension affects the blood flow into the portal vein, which feeds blood to the liver.

Rockey identified the cellular activity that results in portal hypertension. He and his colleagues then took the research a step further, showing that, if the process can be interrupted, the hypertension subsides. "Portal hypertension is a deadly disease that complicates many forms of chronic liver injury," he explains. "When this occurs, in its most severe form, the prognosis definitely becomes guarded," often leading to the need for a liver transplant.

The short-term mortality for patients with portal hypertension is about 30%. The latest research opens new ground and has implications for possible clinical approaches. "The end result of portal hypertension is bleeding and development of ascites [fluid in the abdomen]; so, if you could treat it early, you could prevent bleeding or the formation of ascites," Rockey observes.

Portal hypertension is similar to the widely known essential hypertension--which impairs blood flow to the heart systems--except it affects blood flow to the liver-related systems.

The liver is an essential organ that washes the body's blood of wastes and poisons. Cirrhosis of the liver occurs when the cells are damaged. Scarring often results, reducing blood flow and raising pressure on veins. The high pressure can cause veins to burst, resulting in internal bleeding and, potentially, death.

Previous studies have shown that, at the cellular level, portal hypertension results from reduced production of needed nitric oxide, which regulates expansion of the blood vessels. Rockey's research identifies how the nitric oxide production breaks down due to the effects of the protein GRK2. The protein attaches to another protein called AKT, interrupting the creation of nitric oxide.

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