Review: The role of angiotensin II AT1-receptors in the regulation of the cerebral blood flow and brain ischaemia.

JRAAS 2001;2 (suppl 1):S102-S109 Introduction Cerebral blood flow (CBF) is maintained fairly constantly at about 50 ml/100 g tissue, or approximately 15% of the cardiac output, by effective and unique autoregulatory mechanisms. Autoregulation allows the brain to adapt to rapid changes in peripheral arterial blood pressure (BP) by adequately changing the calibre of the small cerebral resistance vessels and larger cerebral arteries. Within the limits of this autoregulation, increases in BP result in cerebral vasoconstriction, and decreases in BP in cerebral vasodilatation, maintaining the CBF at a constant value. When the mean BP exceeds the upper limit of the autoregulatory range, cerebral vasoconstriction can no longer withstand the pressure, and forced dilation occurs, producing increased CBF, cerebral oedema, and a breakdown of the blood-brain barrier. Conversely, when the mean BP decreases beyond the lower limit of autoregulation, cerebral vasodilatation can no longer compensate and maintain flow, and the CBF precipitously declines.