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ShareNov. 15, 1999 — WINSTON-SALEM, N.C. - The same hormone that causes high blood pressure may promote the development of atherosclerosis, reported researchers from Wake Forest University Baptist Medical Center today (Nov. 9) at the national meeting of the American Heart Association.
The researchers said the protein Angiotensin II, which causes a narrowing of small blood vessels and raises blood pressure, may also promote the buildup of fatty deposits in the arteries of people with high cholesterol.
"It's possible that to prevent the development of plaque buildup, we need to treat not only cholesterol, but to treat the hormone that has been linked to hypertension," said Carlos Ferrario, M.D., director of the Hypertension and Vascular Disease Center, who presented the findings.
In a study of cymomolgus monkeys fed a high-fat diet, the researchers found that the anti-hypertensive drug Losartan inhibited the development of atherosclerosis by 50 percent compared to monkeys that didn't receive the drug.
The monkeys, who did not have hypertension, were selected for study because they have marked similarities to humans in the development of cardiovascular disease.
This was the first study to demonstrate that a drug used to block Angiotensin II and control blood pressure can prevent or slow down the development of atherosclerosis. Researchers believe the effect was caused by the drug's ability to protect low-density lipoproteins, the so-called "bad" cholesterol, from oxidization. Oxidation increases the toxic effect of lipoprotein on arteries.
"These results imply that we should be more aggressive in treating patients with hypertension who are at risk for atherosclerosis," Ferrario said. "They suggest that treatment of hypertension with drugs that selectively block the actions of Angiotensin II will slow down or prevent the development of atherosclerosis."
Ferrario said the results are too preliminary to begin treating non-hypertensive patients with the drug. He said future treatment for patients who have high cholesterol and are at risk for heart attack might include both lipid-lowering and anti-hypertensive drugs. Ferrario called for additional research to duplicate the findings in humans and to understand the mechanisms that cause hypertension and atherosclerosis.
Other members of the research team were William B. Strawn, D.V.M., Mark C. Chappell, Ph.D., and Richard H. Dean, M.D., from the Medical Center and Salah Kivlighn, Ph.D., from Merck & Co., which manufactures Losartan and funded the research.
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The above story is reprinted from materials provided by Wake Forest University Baptist Medical Center.
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