Cerebral Blood Flow in Hypertension

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Abstract
The most important aspect of cerebral blood flow (CBF) in hypertension is the change that occurs in CBF autoregulation: increased cerebrovascular resistance causes the lower and upper limits of CBF autoregulation to be at higher pressure levels. The mechanism seems to be mainly structural thickening and luminal narrowing of cerebral resistance vessels. These adaptive changes, while protecting the brain against high intravascular pressure, render the brain more susceptible to ischemia at low blood pressure. An obvious consequence of the shift in the lower limit of CBF autoregulation in hypertension is that if the hypertensive patient's blood pressure is lowered acutely to “normal” levels, the pressure is below the patient's lower limit of autoregulation and ischemic damage may result. Basically, antihypertensive drugs can be placed into four groups as regards their effects on the cerebral circulation. First are the drugs without any direct effect: in this case, CBF remains constant until pressure reaches the lower limit of autoregulation and then decreases with any further pressure decrease. Diazoxide is in this category. Second are the drugs that directly dilate the small resistance levels in such a way that CBF is higher than normal at every pressure including pressures below the lower limit of autoregulation. However, perfusion may be uneven and autoregulation may be lost; an example of this kind of drug is dihydralazine. Third are the drugs which by α-or ganglion-blockade prevent the sympathetic vasoconstriction of large cerebral arteries (pial and larger), which can compromise CBF during a fall in blood pressure and hence shift the lower limit of autoregulation to a higher pressure than during blockade. This prevention of vasoconstriction at low pressure should be distinguished from large?? artery dilatation at all pressure levels seen in group four Here, large cerebral arteries (extraparenchymal) are di?? lated by releasing them from angiotensin II-induced ton?? with an inhibitor of angiotensin converting enzyme. The resultant increase in pial artery pressure causes a compensatory autoregulatory constriction of the smaller parenchymal resistance vessels, which enhances their ability to dilate at low pressure but compromises their ability to constrict at high pressure. Hence, both the lower and upper limits of CBF autoregulation are acutely reset to lower pressure; an example of this kind of drug is captopril.

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