Researcher offers up ‘new therapeutic target’ for treating high blood pressure

• Bobby Ampezzan

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Heart disease is the No. 1 cause of death in the U.S. Stroke is No. 4. High blood pressure, or hypertension, is a leading risk factor for both, and in North Carolina, more than 1 in 3 adults have it. But not every case can be improved with lifestyle changes and drugs.

Now, a team of researchers at East Carolina University's Brody School of Medicine has made a significant discovery that could lead to more effective treatments for high blood pressure.

The team published its findings in the American Heart Association's Circulation Research, arguably the nation's leading journal for translational cardiovascular research with a five-year journal impact factor greater than 20. The title made the cover of the publication.

"Targeting Kinin B1R Attenuates Hypertension Through AT1R-dependent Mechanisms" identifies a novel therapeutic target - a receptor in the brain, B1R - and sheds new light on the mechanisms driving high blood pressure. It's the result of more than three years of continuous work designing experiments, collecting data, analyzing results and preparing the manuscript.

"It validates years of research effort and collaboration among different laboratories," said Dr. Srinivas Sriramula, whose lab led the investigation. "We've uncovered a new pathway that we can potentially target to better control this widespread and dangerous condition."

"It's an amazing achievement," said fellow researcher Dr. Karen Litwa.

Drug- and Lifestyle-Resistant Hypertension

Not all high blood pressure is created equal. Sympathetic nervous system overactivity - sympathoexcitation - can lead to neurogenic hypertension, a condition often resistant to drug therapies and weight loss.

It has been associated with increased B1R activation in the brain.

Inside the Department of Pharmacology and Toxicology at the Brody School of Medicine, Sriramula's lab has studied and published findings already on B1R in regulating deoxycorticosterone acetate salt hypertension. The lab also identified a causal relationship between angiotensin II (Ang II) stimulation and B1R expression, but whether B1R may affect Ang II-induced hypertension hadn't been answered.

So the research team went to work figuring out how B1R might be modulated in an overactive nervous system contributing to high blood pressure. They blocked the B1R molecule from expressing itself in animal models, and in so doing, reduced high blood pressure and associated inflammation. They then studied hypertensive human patients and found that, likewise, B1R was overexpressed.

Fast Facts

FAMILY: Wife, Lavanya, and daughter, Lasritha, 7

HOME: Winterville

DISSERTATION: Interaction of tumor necrosis factor-alpha and the renin angiotensin system in the pathogenesis of hypertension (2010)

ECU START: 2017

RESEARCH FOCUS: Hypertension, specifically the neurogenerative kind

RESEARCH FUNDING: An R01 grant from the National Heart, Lung and Blood Institute

WHY IT MATTERS: Hypertension is the leading cause of cardiovascular disease and affects nearly half of all American adults. Many patients remain resistant to current treatments. My work not only advances basic medical science but also brings the possibility of new clinical applications closer to reality.

WHY ECU? Research here is growing rapidly, so it's exciting to be part of the momentum. ECU's mission to improve health outcomes in eastern North Carolina aligns perfectly with our research goals. It's a place where science directly connects to community impact.