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Arterial hypertension leads to modification of the cerebral circulation. This results from the changes in the properties of the large arteries, the correlation between large and small arteries, and the local and systemic molecular factors. The current literature indicates several mechanical components that can modify arterial pressure and flow in the brain: 1. Functionally significant arterial stenosis (with reference to the completed or not-completed Willis circle pattern); 2. Elastic properties of the arteries that are transmitted to the microcirculation (vascular wall characteristics and central aortic pressure); including vascular modification by the general atherosclerotic burden; 3. Small vessel dysfunction; 4. Systemic and local biochemical factors that can influence cerebral microcirculation. The microvascular endothelium is the end of the arterial tree - the ultimate target organ, which responds to mechanical and biochemical, systemic, and local molecular stimuli in almost one and the same way. It is modified by systemic vascular and local metabolic requirements. When microvascular endothelium is impaired, a uniform endothelial "response to injury" follows, abnormal neurohormonal and paracrine signaling, which leads to disruption of the blood-brain barrier and the neurovascular coupling, molecular spill out, modification of local and systemic flow, which in turn closes the vicious circle of endothelial impairment. Large arteries' properties influence microvasculature and local endothelial paracrine and mechanical function. The exact correlation between large and small vessels, morphological characteristics of the aorta and cerebral microcirculation is not fully understood. Further studies of this correlation may have potential implications for the clinical practice. In this review, we herein discuss the possible interaction between the characteristics of large arteries, the small cerebral arteries, and the vascular endothelium in terms of the significance of this process for the cerebral perfusion. [ABSTRACT FROM AUTHOR]