We studied whether K+, a potent cerebrovasodilator released by active neurons, participates in the increase in cortical cerebral blood flow (CBF) elicited by stimulation of the cerebellar fastigial nucleus (FN). Rats were anesthetized by continuous administration of halothane (1-3%), paralyzed and artificially ventilated. FN was stimulated electrically (8 s trains, 50 Hz, 5-10 V) through microelectrodes positioned stereotaxically. K+o (mM) was measured in sensory cortex by K(+)-sensitive micropipettes. In some experiments neocortical CBF was monitored continuously by laser-doppler flowmetry. Stimulation of the FN produced significant increases in K+o that averaged 0.91 +/- 0.16 mM (range 0.5-2.9 mM; n = 19) and were confined to sites corresponding to the intermediate cortical laminae (P less than 0.05, ANOVA). To determine whether such K+o elevations were able to produce increases in CBF comparable to those elicited by FN stimulation, cortical K+o was increased by superfusing the sensory cortex with 20-30 mM K+ in Ringer. K+o elevations of 2.8 +/- 0.6 mM increased CBF by 17 +/- 2% (n = 5), an increase considerably smaller than that elicited by FN stimulation in cerebral cortex. We conclude that K+ is unlikely to mediate the cortical cerebrovasodilation. Furthermore, the restricted spatial distribution of the K+o increase indicates that the cortical neural activity evoked by FN stimulation is highly focal. Thus the findings support the hypothesis that, in cortex, the vasodilation is mediated by activation of a restricted group of neural elements, perhaps neurons in laminae III-IV.