University receives $1.8 million to try pinpoint high blood pressure triggers.

A Colorado State University scientist has received $1.8 million from the U.S. National Institutes of Health to investigate molecular functions that trigger hypertension in people with obesity. His five-year research project could shed light on how oxidant and calcium signals influence blood vessel functions that regulate blood flow and pressure – functions that could contribute to cardiovascular diseases (CVD) such as hypertension, stroke, and coronary artery disease.

Gregory Amberg, an associate professor at CSU’s Department of Biomedical Sciences, said in a press statement that he hopes his research will help define underlying causes of cardiovascular disease ― insight that could provide a focus for better preventive therapies.

“Hypertension is one of the major modifiable risk factors for CVD, but it often goes undiagnosed until it is in the more advanced stages, when the damage is already done,” Amberg said. He added that identifying molecular switches could help prevent high blood pressure and thereby heart disease. This would help avoid organ damage caused by established disease and might help avoid side-effects of some antihypertensive medications. Calcium channel blockers, one current therapy, come with several undesirable side-effects and risks.

His specific interests are the workings of calcium ion channels and their connection to oxidative stress. Calcium ion channels allow calcium to permeate the body’s tissues, triggering smooth muscle to constrict the arteries ― this process increases blood pressure. A rise in oxidative stress often goes hand-in-hand with a rise in calcium influx, which means excess oxygen from metabolic processes, which damages cells.

Amberg wants to understand what causes calcium channel and oxidative signals to go wrong. “My research is showing that there is a linked, reciprocal relationship between two fundamental cell signaling modalities – oxidation and calcium influx – and that increases in these signals may be very early events involved with the development of hypertension,” he said. “I’m trying to understand how reactive oxygen species operate in healthy cells and identify the events that underlie the transition from normal oxidative signaling to overt oxidative stress in pathophysiological conditions associated with disease.”

He adds that understanding underlying mechanisms will help identify new targets for antihypertensive therapy, which is especially important given that CVD is the leading cause of death in the United States.

 

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