page 3159), permitting vessels to adjust their size to match changes in blood flow.
In response to changing demands for blood flow, arteries alter their size to maintain constant tension in their walls. They enlarge when more blood is needed, for example in response to organ growth; and they narrow when demand for blood flags, such as in the uterine arteries after birth. Previous studies had shown that inflammation spurs remodeling of the vessel wall in atherosclerosis and hypertension, but whether inflammation also triggered the responses of healthy arteries to changes in blood flow was not certain.
To test this idea, the team partially tied off one branch of the carotid artery in mice, cutting blood flow by roughly half. Downstream from this obstruction, the artery narrowed by about 10–15%, and smooth muscle cells disappeared to prevent the vessel wall from thickening. The revamping vessel also showed clear signs of inflammation. Cells of the arterial wall churned out inflammation-promoting cytokines and chemokines, drawing in macrophages and other leukocytes. Destroying the animals' macrophages thwarted the restructuring.
Neither inflammation nor remodeling could occur without MyD88, an adaptor protein necessary for cytokine production in response to IL-1 or Toll-like receptor signals. The researchers also discovered that this type of arterial inflammation clears up after about two weeks, which might explain why previous studies didn't detect it.