Improving the Understanding of How Hypertension Results in Vascular Restructuring
The chronic raised blood pressure of hypertension is both (a) driven by the stiffening of blood vessel walls and (b) causes further detrimental restructuring of blood vessel walls, such as thickening of the intimal and medial layers. Researchers here explore the chains of cause and effect that lead to this outcome, mediated by increased inflammatory signaling and the presence of macrophages drawn into the blood vessel walls.
Persistent hypertension can cause long-lasting changes in the structure of vascular smooth muscle cells (the cells making up the walls of blood vessels) through a process called "vascular remodeling." If left unchecked, this restructuring can stiffen arterials walls, which lose their ability to adjust their size appropriately. This, in turn, leads to arteriosclerosis and increases the risk of cerebrovascular disease.
Why and how hypertension triggers vascular remodeling is not entirely clear. Scientists have shown that macrophages, a type of white blood cells that kill foreign bodies, are involved in the transformation. Specifically, the macrophages accumulate within blood vessel walls from outside the vessels and cause chronic inflammation. However, the underlying mechanism that orchestrates this process remains unknown.
A new study recently investigated a mechanism known as "excitation-transcription (E-T) coupling" in vascular smooth muscle cells. Although E-T coupling occurs in vascular smooth muscle cells after an influx of Ca2+ under high pressure, not much was known about how it happens, what genes are triggered, and the role it plays in our bodies.
By taking a detailed look at the genes promoted by E-T coupling and observing their effects when blocked or amplified, the researchers made some important discoveries. Firstly, some of these genes were related to chemotaxis, the phenomenon by which cells movement is triggered and directed by chemical stimuli. This helped explain the accumulation of macrophages in blood vessel walls from outside the vessels. Additionally, these genes promoted the remodeling of the medial layer of arteries, where vascular smooth muscle cells reside and control blood flow through contraction and expansion. "Taken together, our results explain how E-T coupling caused by high pressure in vascular smooth muscle cells can modulate macrophage migration and subsequent inflammation, altering the vascular structure,"