Contribution of potassium channels to active XXXX of the @entity235 diaphragm.

@entity3855 @entity3529 @entity19191 @entity235 @entity5217 @entity450 @entity3612 @entity141 @entity3352 @entity855
@entity5217 , @entity19191 , and apamin (blockers of @entity855 -sensitive, large-conductance, and small-conductance @entity141 -activated @entity3529 channels, respectively) were infused into the diaphragmatic vasculature of anesthetized @entity3352 -treated @entity235 to assess the contribution of @entity3529 channels to active @entity450 . Diaphragmatic blood flow (Qphr) and @entity3612 uptake (VO2di) were measured at rest and during 2 min of continuous left phrenic nerve stimulation at 0.5, 1, 2, and 4 Hz. These measurements were repeated before (control) and after the infusion of a selective @entity3529 channel blocker in three groups of animals. @entity5217 at 10(-5) M significantly attenuated Qphr at rest and in response to all stimulation frequencies. Whereas resting VO2di remained unchanged, @entity5217 infusion significantly reduced VO2di in response to all stimulation frequencies. The slope of the linear relationship between Qphr and VO2di, however, was not affected by @entity5217 . By comparison, infusion of @entity19191 (10(-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. @entity3855 (10(-6) M) infusion in a third group reduced only resting Qphr with no effect on active @entity450 during phrenic nerve stimulation. Neither @entity19191 nor apamin influenced resting or stimulated VO2di. In all groups diaphragmatic tension measured after the infusion of @entity3529 channel blockers remained similar to control values. These results indicate that @entity3529 channels, especially those sensitive to @entity5217 , modulate the increase in Qphr and VO2di in response to moderate augmentation of metabolic demands.
