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OHSU Study Shows That A Molecule Critical To Nerve Cells Increases Drammatically During Hypertension

Researchers at Oregon Health & Science University’s School of Dentistry have made an important connection between a molecule critical to and . Production of the molecule Brain-Derived Neurotrophic Factor () appears to increase dramatically in blood pressure-sensing nerve cells during . The study, published online in the Journal of Neuroscience Research, may someday have implications for the prevention and treatment of high blood pressure, which affects about one in three adults in the United States.

BDNF is essential to the normal development and plasticity of nerve cells. Using two distinct hypertensive animal models, team data suggest a direct role of BDNF in regulation of blood pressure.

“We are now able to knock down BDNF in the blood pressure control system and can move toward answering the next critical question, which is whether BDNF contributes to the development of hypertension, or whether it provides a compensatory mechanism counteracting those that lead to hypertension” said Agnieszka Balkowiec, M.D., Ph.D., associate professor of integrative biosciences, OHSU School of Dentistry, and adjunct assistant professor of physiology and pharmacology, OHSU School of Medicine, whose lab teamed with Virginia Brooks, Ph.D., professor of physiology and pharmacology in the OHSU School of Medicine.

Previous studies from Balkowiec’s lab showed that BDNF is made by blood pressure-sensing nerve cells called ‘baroreceptors’. BDNF is released from the baroreceptors onto relay cells in the brainstem when nerve activity rises, as in hypertension


Additional study authors include: Anke Vermehren-Schmaedick, Ph.D., research associate, OHSU Department of Biomedical Engineering; Victoria K. Jenkins, a doctoral student at Boston University; Hui-ya Hsieh, a research associate at the University of Alabama; Alexandra Brown, an undergraduate student at Brown University; and Mollie P. Page, a research assistant for Dr. Brooks.

The research was supported by grants from the American Heart Association, Medical Research Foundation of Oregon, and the National Institutes of Health’s National Heart, Lung, and Blood Institute (under Award Numbers HL076113, HL070962 and HL088552), including the American Recovery and Reinvestment Act. The content of the publication is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Oregon Health & Science University