Inhibition of @entity4 after XXXX -reperfusion by b-adrenergic antagonists: correlation with increased K+ and decreased @entity141 concentrations in extracellular fluid.

@entity2657 @entity63 @entity4 @entity141 @entity2161 @entity17365 @entity1188 @entity3044 @entity4338
@entity1188 size and @entity2657 following @entity63 /reperfusion are reduced by inhibitors of the Na+, K+, 2Cl-, and water cotransporter @entity17365 and by @entity2161 antagonists. @entity17365 is a secondary active transporter, mainly localized in astrocytes, driven by transmembrane Na+/K+ gradients generated by the Na+,K+-ATPase. The astrocytic Na+,K+-ATPase is stimulated by small increases in extracellular K+ concentration and by the b-adrenergic agonist @entity3044 . Larger K+ increases, as occurring during @entity63 , also stimulate @entity17365 , creating cell swelling. This study showed no @entity4 after 3   hr medial cerebral artery occlusion but pronounced @entity4 after 8   hr reperfusion. The @entity4 was abolished by inhibitors of specifically b1-adrenergic pathways, indicating failure of K+-mediated, but not @entity2161 -mediated, stimulation of Na+,K+-ATPase/ @entity17365 transport during reoxygenation. Ninety percent reduction of extracellular @entity141 concentration occurs in @entity63 . @entity141 omission abolished K+ uptake in normoxic cultures of astrocytes after addition of 5   mM @entity4338 . A large decrease in ouabain potency on K+ uptake in cultured astrocytes was also demonstrated in @entity141 -depleted media, and endogenous ouabains are needed for astrocytic K+ uptake. Thus, among the ionic changes induced by @entity63 , the decrease in extracellular @entity141 causes failure of the high-K+-stimulated Na+,K+-ATPase/ @entity17365 ion/water uptake, making b1-adrenergic activation the only stimulus and its inhibition effective against @entity4 .
