AHEART March 47/3

Nguyen, Thien-Son, H. Richard Winn, and Damir Janigro. ATP-sensitive potassium channels may participate in the coupling of neuronal activity and cerebrovascular tone. Am. J. Physiol. Heart Circ. Physiol. 278: H878–H885, 2000.—K1 dilate and constrict cerebral vessels in a dosedependent fashion. Modest elevations of abluminal K1 cause vasodilatation, whereas larger extracellular K1 concentration ([K]out) changes decrease cerebral blood flow. These dilations are believed to be mediated by opening of inwardrectifier potassium channels sensitive to Ba21. Because BaCl2 also blocks ATP-sensitive K1 channels (KATP), we challenged K1 dilations in penetrating, resistance-size (,60 mμ) rat neocortical vessels with the KATP channel blocker glibenclamide (1 μM). Glibenclamide reduced K1 responses from 138 6 8 to 110 6 0.8%. K1 constrictions were not affected by glibenclamide. The Na1-K1-pump inhibitor ouabain (200 μM) did not significantly change resting vessel diameter but decreased K1 dilations (from 153 6 9 to 99 6 2%). BaCl2 blocked K1 dilations with a half-maximal dissociation constant of 2.9 μM and reduced dilations to the specific KATP agonist pinacidil with equal potency. We conclude that, in resistance vessels, K1 dilations are mediated by KATP; we hypothesize that [K]out causes activation of Na1-K1 pumps, depletion of intracellular ATP concentration, and subsequent opening of KATP. This latter hypothesis is supported by the blocking effect of ouabain.