There have been major advances in our understanding of regulation of cerebral circulation under normal conditions, and of cerebral vascular changes during hypertension. In relation to physiological mechanisms, nitric oxide (NO), or an NO-containing substance, appears to play an important role in regulation of cerebral blood flow, including coupling of metabolism and blood flow. ATP-sensitive potassium channels are a major mechanism that mediates cerebral vasodilatation during several pharmacological and physiological stimuli, including hypoxia. In relation to hypertension, potent mechanisms protect the cerebral circulation during chronic hypertension. Vascular hypertrophy also protects cerebral vessels during hypertension by reducing wall stress and by attenuation of increases in pressure in the microcirculation. Vascular remodeling, which results in reduction in external diameter of cerebral vessels, appears to be the dominant structural change in cerebral arterioles during hypertension. Endothelial dysfunction may play a key role in cerebral vascular complications of hypertension. It is now thought that hypertensive encephalopathy is produced by dysfunction of the endothelial blood-brain barrier. Endothelial dysfunction in chronic hypertension also results in abnormal vasomotor regulation. Cerebral vascular muscle also may be dysfunctional in hypertension, as responses to activation of ATP-sensitive potassium channels appear to be impaired. Several mechanisms may predispose to stroke as a complication of hypertension. Endothelial dysfunction may lead to vasospasm, for example, when platelets are activated. Collateral circulation in the cerebrum is impaired by hypertension. Mean pressure is higher in arterioles in the brain stem than in cerebral cortex, which may predispose to hemorrhage in the brain stem.
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