CONSTRICTION of cerebral arterioles has recently been observed over areas of experimental infarction.1,2 The mechanism of this constriction is not understood, but it has been stated that the segmental constriction illustrated in these reports2 does not resemble passive collapse due to reduced perfusion pressure.1 Instead, it has been suggested that some chemical agent is released from the ischemic tissue, and that this hypothetical substance produces the constriction observed.1 Since perfusion pressure is reduced in the area of infarction, it occurred to us that at least one other factor might account for the vasoconstriction beside the regional release of a vasoconstrictor. This factor would be an increased sensitivity of the vessels to a constricting influence. Although many publications have been written about the effect of altered pressure on vascular diameter3,4 and about the effects of chronic hypertension on cerebrovascular reactivity,4 we could find no