Vascular ATP-sensitive K+ (KATP) channel activation enhances exercise-induced hyperemia.
We examined the effect of KATP channel inhibition via glibenclamide on microvascular O2 driving pressure (PO2mv) kinetics following the onset of contractions.
Glibenclamide caused an undershoot of PO2mv, nearly doubled the time to reach the contracting steady-state and reduced the overall mean PO2mv.
This effect raises the question of whether muscle vascular KATP channel dysfunction underlies, in part, the clinical manifestations (e.g., exercise intolerance) associated with the use of sulphonylureas in the treatment of diabetes mellitus.