BOSTON -- Alterations in blood vessel dilation lie at the heart of coronary artery health: When vessels dilate, blood and oxygen supplies successfully reach the heart. When vessels contract, blood and oxygen are diminished, leading to coronary artery disease.
The biology behind this course of events, known as vasodilation, occurs through nitric oxide, a gaseous molecule synthesized by an enzyme called eNOS, which relaxes the vascular smooth muscle cells lining the outer layer of coronary vessels. If, during this course of events, nitric oxide (NO) encounters another group of molecules known as reactive oxygen species (ROS), then NO is inactivated, and instead of dilating, blood vessels contract. In other words, ROS are harmful.
But a paper by Ruhul Abid, MD, PhD, of BIDMC's Center for Vascular Biology Research upends this long-held notion, demonstrating that ROS has another, beneficial role in the activation of eNOS and the nitric oxide production process and, in fact, is necessary to maintain coronary vasodilation.
This paradoxical discovery, published last spring in the American Heart Association journal Arteriosclerosis, Thrombosis, and Vascular Biology, was recently selected from more than 650 entries as the journal's most outstanding Vascular Biology paper of 2010. Abid will receive the AHA's 2011 Werner Risau New Investigator Award in Vascular Biology on April 29 in Chicago for this groundbreaking work.
"ROS are generally believed to play harmful roles in microvascular tone in hypertension, angiogenesis and vascular complications of arthritis and diabetes," explains Abid. "As a result, it's been widely assumed that by reducing ROS oxidants, you can improve cardiovascular function." In fact this is the premise underscoring the use of antioxidants, such as Vitamins E and C and beta carotene, to help prevent heart disease.
"But our findings now suggest that these high oxidant levels often found in the
|Contact: Bonnie Prescott|
Beth Israel Deaconess Medical Center