Functional evidence for inward-rectifier potassium channels in rat cremaster muscle arterioles

Abstract

Moderate increases in extracellular K+ produce vasodilation in fourth order cremasteric arterioles in the anesthetized rat. We studied the contribution of different subtypes of K+ channels to this response. Cremaster muscle arteriolar diameters were observed during superfusion with buffer containing 5-30 mM K+ in the absence (control) and presence of barium (Ba2+, 50 μM), glibenclamide (GLIB, 1 μM), or iberiotoxin (IBTX, 100 nM) to block inward-rectifier, ATP-sensitive, or Ca2+-activated K+ channels, respectively. Under control conditions, vessels dilated in response to 10-25 mM K+ and constricted at higher concentrations. At 5 mM K+, vessel diameters were significantly decreased by GLIB and Ba2+, but not IBTX, suggesting that basal diameter was regulated by inward-rectifier and ATP- sensitive K+ channels. In contrast, Ba2+, but not GLIB or IBTX, prevented K+-induced dilation. The data indicate that the inward-rectifier K+ channel (blocked by low concentrations of Ba2+, but not GLIB or IBTX) was most likely responsible for the K+induced arteriolar dilation. (C) 2000 Academic Press.