Research / Discovery

Researcher investigates the triggers for hypertension

November 20, 2013
by Kerri McDermid

A Colorado State University scientist has received $1.8 million from the National Institutes of Health to investigate molecular functions that trigger hypertension in people with obesity.

Gregory Amberg, an associate professor in the CSU Department of Biomedical Sciences, hopes his research will help define underlying causes of cardiovascular disease, insight that could provide a focus for better preventative therapies.

“Hypertension is one of the major modifiable risk factors for cardiovascular disease, but it often goes undiagnosed until it is in the more advanced stages, when the damage is already done,” Amberg said.

Identifying molecular switches could help prevent hypertension, and thus heart disease; this would help to avoid organ damage that often accompanies established disease, and might help avoid side-effects of some current antihypertensive medications, he said.

Striving for better preventative therapies

Amberg’s specific interests are the workings of calcium ion channels and their connection to oxidative stress.

Gregory Amberg is investigating molecular triggers for hypertension and heart disease.Calcium ion channels allow calcium to permeate the body’s tissues, triggering smooth muscle to constrict the arteries – a process that increases blood pressure. Often accompanying a rise in calcium influx is a rise in oxidative stress, meaning an overabundance of oxygen from metabolic processes, which is damaging to cells, Amberg said.

“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.”

Amberg wants to understand what causes calcium channel and oxidative signals to go awry. His five-year research project, funded by the NIH,  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 such as hypertension, stroke, and coronary artery disease.

“Understanding underlying mechanisms will ideally help us to identify new targets for antihypertensive therapy,” he said.

That’s significant, given that cardiovascular disease is the leading cause of death in the United States. Likewise, calcium channel blockers, one current therapy, come with some unwanted side-effects and risks. 

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