University of Southwestern is reporting that a research team has " identified mechanisms causing a potentially deadly type of hypertension that results from liver damage - findings that could lead to its prevention."

Dr. Don Rockey, the new chief of the digestive and liver diseases division at UT Southwestern, 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.

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.

Dr. Rockey's research identified 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.

"We've shown that the endothelial cells that line the blood vessels in the liver don't work quite right. Specifically, they don't produce nitric oxide," Dr. Rockey said. "The problem is that there are a number of signaling pathways that are disrupted and that results in the reduced production of nitric oxide."

In addition to identifying how the system breaks down, Dr. Rockey's study showed that reducing the GRK2 production restored AKT production, allowing nitric oxide levels to stabilize and blood pressure to return to normal.

Further research will be needed, Dr. Rockey said, to determine how to control GRK2 proteins that interfere with AKT or ways to bolster AKT protein production to maintain nitric oxide production.

News release link to southwestern univ site