CONTRIBUTION OF POTASSIUM CHANNELS TO ACTIVE HYPEREMIA OF THE CANINE DIAPHRAGM

Contribution of potassium channels to active hyperemia of the canine d iaphragm. J. Appl. Physiol. 76(3): 1098-1105, 1994. - Glibenclamide, i beriotoxin, and apamin (blockers of ATP-sensitive, large-conductance, and small-conductance Ca2+-activated K+ channels, respectively) were i nfused into the diaphragmatic vasculature of anesthetized indomethacin -treated dogs to assess the contribution of K+ channels to active hype remia. Diaphragmatic blood flow (Qphr) and O-2 uptake (VO2di) were mea sured at rest and during 2 min of continuous left phrenic nerve stimul ation at 0.5, 1, 2, and 4 Hz. These measurements were repeated before (control) and after the infusion of a selective K+ channel blocker in three groups of animals. Glibenclamide at 10(-5) M significantly atten uated Qphr at rest and in response to all stimulation frequencies. Whe reas resting VO2di remained unchanged, glibenclamide infusion signific antly reduced VO2di in response to all stimulation frequencies. The sl ope of the linear relationship between Qphr and VO2di, however, was no t affected by glibenclamide. By comparison, infusion of iberiotoxin (1 0(-7) M) in a second group reduced Qphr at rest and in response to 0.5 - and 1-Hz stimulation, whereas Qphr measured in response to 2- and 4- Hz stimulation remained similar to control values. Apamin (10(-6) M) i nfusion in a third group reduced only resting Qphr with no effect on a ctive hyperemia during phrenic nerve stimulation. Neither iberiotoxin nor apamin influenced resting or stimulated VO2di. In all groups diaph ragmatic tension measured after the infusion of K+ channel blockers re mained similar to control values. These results indicate that K+ chann els, especially those sensitive to glibenclamide, modulate the increas e in Qphr and VO2di in response to moderate augmentation of metabolic demands.