When Andrea Eckhart, Ph.D., associate professor of medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia, and her co-workers turned up the volume on GRK5, overexpressing a mouse gene that makes the protein, the researchers saw extreme rises in blood pressure even when the animals were resting.
Not only that, they found that high blood pressure segregated with gender. That is, female mice with an overexpressed GRK5-making gene had a lesser spike in blood pressure than males, which Dr. Eckhart says, has intriguing implications.
"This difference suggests it could be a great model for human hypertension, especially for premenopausal women," says Dr. Eckhart, who is director of the Eugene Feiner Laboratory in the Center for Translational Medicine in the Department of Medicine at Jefferson Medical College. "Is the difference due to a protective effect of estrogen, or because males with testosterone make it worse? We're now looking at the effects of these androgens in conferring differences."
Dr. Eckhart thinks it could be a "powerful hypertensive model to look at different new hypertensive therapies that different drug companies come up with to look at the effects of estrogen."
To Dr. Eckhart and her group, which reported their results August 23, 2005 in Circulation, a journal of the American Heart Association, the finding is another step in the laboratory's goal of uncovering the molecular roots of hypertension. More than 90 percent of cases can't be pinned to a particular molecular cause.
GRK5, short for G-coupled protein receptor kinase, was known to rise in animal models with high blood pressure. According to Dr. Eckhart, this kinase acts as a switch that essentially turns off receptors. Such receptors bind catecholamin
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5-Oct-2005