Work is now under way to locate and identify the hormone, which is believed to be produced in very small, but highly potent amounts, so that its hypertension-causing action can be blocked.

Finding and neutralizing this "new player" in the mechanism of hypertension, the UC scientists said, could provide a breakthrough in the prevention of preeclampsia--which so far has been essentially untreatable--and other hypertensive conditions.

One of the Cincinnati research team's areas of interest, preeclampsia is a leading cause of fetal complications, which include low birth weight, premature birth and stillbirth. It can lead to seizures, known as eclampsia, the second leading cause of maternal death in the United States.

The researchers, Jerry Lingrel, PhD, chair of the University of Cincinnati's Department of Molecular Genetics, Biochemistry and Microbiology, and Iva Dostanic-Larson, PhD, a postdoctoral fellow in the department, report the findings of their three-year study in the Oct. 17, 2005, online edition of the Proceedings of the National Academy of Sciences (PNAS).

The work was funded by grants from the U.S. National Institutes of Health (NIH) and the Heart and Stroke Foundation of Ontario.

The focus of their research, said Dr. Lingrel, the principal investigator, is an area in the human cell known as the "sodium pump," an enzyme (Na,K-ATPase) that has long been known to be involved in the regulation of blood pressure, excitability of muscle and nerve tissue and the uptake of a wide range of essential nutrients.

The sodium pump contains the target or "binding site" of a group of drugs called cardiac glycoside
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Contact: David Bracey
david.bracey@uc.edu
513-558-4559
University of Cincinnati
17-Oct-2005