Hydrogen Sulfide Key Player in Blood Pressure Regulation

Mouse study finds 'rotten egg'-smelling gas relaxes arteries, may have broader applications

THURSDAY, Oct. 23, 2008 (HealthDay News) -- Cells inside the blood vessels of mice -- and probably humans -- naturally make the gas hydrogen sulfide, which helps regulate blood pressure by relaxing blood vessels, according to an international team of scientists.

"Now that we know hydrogen sulfide's role in regulating blood pressure, it may be possible to design drug therapies that enhance its formation as an alternative to the current methods of treatment for hypertension," study co-author Dr. Solomon H. Snyder, a neuroscientist at Johns Hopkins University, said in a Hopkins news release.

The study included mice missing a gene for an enzyme called CSE, long believed to be responsible for the production of hydrogen sulfide. When the researchers compared hydrogen sulfide levels in the CSE-deficient mice and normal mice, they found the gas was largely depleted in the cardiovascular system of the CSE-deficient mice. This shows that tissue in mammals normally use CSE to make hydrogen sulfide, the researchers said.

The researchers also found that CSE-deficient mice had blood pressure spikes of about 20 percent, comparable to serious hypertension in humans.

In another test, the researchers studied how blood vessels in CSE-deficient mice responded to the neurotransmitter methacholine, known to relax normal blood vessels. The blood vessels in the CSE-deficient mice showed little response, indicating that hydrogen sulfide plays a major role in blood vessel relaxation.

The findings, published Oct. 23 in the journal Science, may have broad applications to human physiology and disease, Snyder said.

"In terms of relaxing blood vessels, it looks like hydrogen sulfide might be as important as nitric oxide," which two decades ago was discovered to regulate blood pressure, Snyder said.

More information

The American Heart Association has more about high blood pressure.

SOURCE: Johns Hopkins Medicine, news release, Oct. 23, 2008
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