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Researchers Find Gene Implicated in High Blood Pressure

Discovery could lead to preventative treatments

January 14, 2008

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Millions of people have high blood pressure, putting them at increased risk of heart attack and stroke. Some causes may be obvious – obesity, too little exercise, too much sodium in the diet – others not so obvious.

Now, scientists say they may have determined why so many seemingly healthy adults struggle with dangerously high blood pressure.

They point to a gene that sets off a sequence of events in the blood vessels, eventually making conditions in vessels ripe for the creation of blockages that can cause heart attacks, strokes and circulatory problems.

The finding in a study led by Ohio State University researchers might lead to new therapeutic options for high blood pressure, especially hypertension associated with aging. Obesity and aging contribute to increasing cases of high blood pressure, which currently affects an estimated 50 million Americans.

Despite more intensive treatments available for hypertension, little has been done to prevent it.

A change in the structure of the blood vessels, called vascular remodeling, increases with age and triggers the onset of the disease. When remodeling occurs, blood vessel walls increase in thickness, decreasing the diameter of the channel through which blood normally flows.

The gene, called profilin 1, has been traced to a series of interactions within the smooth muscle cells of blood vessels that causes those cells to increase in size. This in turn narrows the channel through which blood flows, causing stress on vessel walls, injuring the lining of the vessel walls and making it easier for blockages to develop.

By identifying this pathway, researchers say they hope to pinpoint the most effective therapeutic target to interfere with the disease process.

The researchers used genetically altered mice that produce excessive amounts of the human profilin 1 gene in the vascular smooth muscle cells and observed the changes to the vessels that followed, which led to high blood pressure by the time the mice were 6 months old – the rough equivalent to middle age in humans.

"We created the disease in the animals and then went backwards to understand how the disease developed," said Hamdy Hassanain, assistant professor of anesthesiology at Ohio State University and senior author of the study.

"This is an important finding because vascular disease originates in the smooth muscle cells, which have significant impact on the dysregulation of blood pressure that leads to heart disease."

Blood vessels contain three important layers – the endothelium that lines the vessel walls, the smooth muscle cells responsible for regulating blood flow, and the lumen, the open channel through which blood travels.

In healthy young humans, the production of compounds by the cells in these layers remains balanced, allowing for normal vessel function and unrestricted blood flow.

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