The contribution of vasodilator cyclooxygenase (COX) metabolites to the maintenance of the cerebrocortical blood flow (CBF) has been studied under physiological conditions and in nitric oxide (NO) deficiency. Inhibition of COX decreased resting CBF without changing arterial blood pressure. NO synthase blockade resulted in hypertension and CBF reduction as well as in enhanced cerebral prostacyclin and prostaglandin E2 production. Despite the increased vasodilator prostanoid release in the absence of NO, the CBF-decreasing effect of COX blockade failed to increase. Therefore, the COX pathway seems to play a similar role under physiological and NO-deficient conditions in the maintenance of the resting CBF.
Animals Blood Pressure