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

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 (Ba(2+), 50 microM), glibenclamide (GLIB, 1 microM), or iberiotoxin (IBTX, 100 nM) to block inward-rectifier, ATP-sensitive, or Ca(2+)-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 Ba(2+), but not IBTX, suggesting that basal diameter was regulated by inward-rectifier and ATP-sensitive K(+) channels. In contrast, Ba(2+), but not GLIB or IBTX, prevented K(+)-induced dilation. The data indicate that the inward-rectifier K(+) channel (blocked by low concentrations of Ba(2+), but not GLIB or IBTX) was most likely responsible for the K(+)-induced arteriolar dilation.