Vascular stiffening is a major cause of cardiovascular aging. It alone is enough to explain the age-related onset of hypertension, for example, which in turn deforms blood vessels and the heart, and causes ongoing harm to the brain where small blood vessels fail under stress, among other issues. Much of the cause of loss of elasticity in blood vessels is thought to be caused by cross-linking and calcification in the extracellular matrix, processes that occur as a side-effect of the normal operation of metabolism, and which could be reversed with suitably designed drugs. Unfortunately there is still comparatively little research focused on these targets, certainly nowhere near as much as is merited by the consequences of these contributing causes of degenerative aging.
Here, researchers identify another potential causative agent in the stiffening of blood vessels, in changing behaviors and characteristics of the smooth muscle cells that surround blood vessels. Is this a primary cause or a reaction to primary causes, however? More research is needed on that topic, as is often the case:
Arterial and vascular stiffness occurs through the normal process of biological aging and is associated with an increased risk of heart attacks and strokes. As we age, the aorta, which normally acts as a shock absorber dampening the pulse associated with each heartbeat, tightens and becomes rigid, causing a host of problems including high blood pressure, increased risk of adverse cardiovascular events and even death. In the United States, the risk of developing hypertension due to aging is greater than 90 percent in both men and women. Recent studies have identified several mechanisms for arterial stiffness in humans. Research has focused on the structural matrix proteins, or non-living components that compose the outer walls of blood vessels, as well as endothelial cells which line the inner portion of the vascular walls.
Researchers have focused on a new potential source - smooth muscle cells that are a major component of the "middle" of the blood vessel wall. The team isolated aortic cells from normal and hypertensive rat models in both young and aged animals. Then, using atomic force microscopy, an advanced microscope that incorporates a tiny probe that can interact with single cells and molecules, the team measured the compression force of the needle against the specimen and how the tip adhered to or "stuck" to smooth muscle cells.
"We found that hypertension increased both vascular smooth cell stiffness and adhesion or stickiness, and that these changes were augmented by aging. Our results are adding to our understanding and taking studies in a different direction. Although all cells are contributing to arterial stiffness, it's important to identify the order in which they're adding to the problem. Identifying smooth muscle cells as a contributor can help identify possible preventatives and potential drugs to counteract and reverse the disease and keep vessels healthier as we age."