Arterial stiffness and the brain

Abstract

In healthy humans, brain perfusion is adequately regulated, minute-tominute, to match flow and neuronal metabolic demand, while cerebral blood flow (CBF) is maintained somewhat constant in the face of a variable systemic blood pressure between periods of sleep and of high intensity exercise. Vascular wall stiffness may impair CBF in pathological conditions such as hypertension or chronic kidney disease and in physiological condition such as aging. Little is known about changes in intracranial vessels stiffness during aging, hypertension, or chronic kidney disease. Cerebral arteries show an increase, a decrease, or no change in distensibility following the conditions and depending on vessel size. It is also well known that peripheral arteries stiffness may have an impact on CBF and lead to brain damages, the so-called pulse wave encephalopathy. Cerebral vessels are low resistance vessels and the pulse wave is transmitted through capillaries to the venous system. Any increase in pulse wave may thus lead to alteration in the neurovascular unit (endothelial cell/astrocyte/neuron) and brain function. This chapter aims at summarizing our knowledge on the interaction between (peripheral) arteries stiffness and brain. We will first summarize the main characteristics of brain vessels before describing pulse wave encephalopathy and emphasizing the potential role of endothelium in the development of cerebral alterations. As stiffness of peripheral arteries may contribute to chronic hypoperfusion, neuronal death, and the cognitive decline observed in hypertension, chronic kidney disease, and aging, this may open the door for potential treatments of these disorders. Drugs that decrease arterial stiffness may prevent or delay cognitive impairment.