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Nitric Oxide Helps Keep Atherosclerosis in Check
Excerpt from "Blood Vessels and Aging: The Rest of the Journey"
Aging, for instance, triggers thickening of the intima and stiffening of the arterial walls. This occurs, in part, because of a fierce molecular struggle.
Healthy endothelial cells produce nitric oxide, an important signaling molecule that helps keep arteries supple. When nitric oxide enters a cell, it stimulates a biochemical process that relaxes and dilates blood vessels. Nitric oxide also helps keep atherosclerosis in check by preventing platelets and white blood cells from sticking to the blood vessel walls. The molecule also can curb the abnormal growth of vascular muscle, which can thicken blood vessel walls.
But unhealthy endothelial cells are a different story. In these cells, nitric oxide regulation is impaired. To make nitric oxide, endothelial cells need L-arginine, an amino acid that is one of the basic building blocks of proteins, and an enzyme called nitric oxide synthase (NOS). Normally, endothelial cells have plenty of L-arginine and NOS. But NOS is often in short supply in aging blood vessels.
In addition, people who have heart disease or who are at high risk of developing it produce a modified amino acid called asymmetric dimethylarginine (ADMA). ADMA blocks the production of nitric oxide from L-arginine. Even if sufficient amounts of nitric oxide are produced, it can be inactivated by oxygen free radicals, unstable molecules that injure vascular tissue. In any case,without adequate levels of biologically available nitric oxide, endothelial cells in the intima can't function properly.
In fact, some researchers consider decreased availability of nitric oxide in the endothelium as one of the earliest signs of arterial aging and a pathological sign of atherosclerosis and high blood pressure. However, much of this complex process remains a mystery and scientists continue to explore precisely how nitric oxide production and bioavailability affect blood vessels.
Nitric oxide helps subdue the production of oxygen free radicals
But they do know that endothelial cells depend on nitric oxide to help subdue the production of oxygen free radicals. Nitric oxide molecules can eradicate some of these free radicals, but in the process they also destroy themselves. This leaves less nitric oxide available to help endothelial cells keep arteries in tiptop shape.
Angiotensin II, a growth factor involved in this process, is more prevalent in aging arteries. In addition to increasing free radical production, angiotensin II decreases nitric oxide production and stimulates blood vessel inflammation. It also can cause vessels to tighten and raise blood pressure, forcing the heart to work harder.
Much of angiotensin II's damage is done in partnership with an enzyme called NADPH oxidase, the primary source of free radicals in the arteries. After angiotensin II activates it, NADPH oxidase causes an increase in production of superoxide, a free radical. Superoxide binds with nitric oxide to create an even more potent free radical called peroxynitrite. Peroxynitrite then binds to proteins and nitrites, harming them. Like other free radical processes, this chain of events steals bioavailable nitric oxide away from endothelial cells, leaving them more vulnerable to damage. But the impact of angiotensin II isn't limited to the intima. It also has an important role in age-associated alterations of the media, the middle layer of the arterial wall.
In addition to depleting nitric oxide, free radicals can damage the membranes and DNA of endothelial cells in the intima and smooth muscle cells in the media. Free radical damage is one of many things that can induce some of these cells to stop functioning, shrink, and ultimately die in a process known as apoptosis. Apoptosis may contribute to the decline in cardiovascular health as we age. Free radicals also can oxidize proteins, altering their structure and function. As a result, these proteins can't work properly, and this can trigger a cascade of cellular alterations that promote stiffening and thickening of arterial walls and contribute to atherosclerotic plaque build up.
Keywords: Nitric Oxide, atherosclerotic plaque, Atherosclerosis, intima, stiffening of the arterial walls, aging, antiaging, endothelial cells, L-arginine, amino acid, NOS, high blood pressure, arterial lumen, aventitia, free radicals, inflammation, apoptosis, heart attack, stroke
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