FUNCTIONAL HYPEREMIA IN STRIATED-MUSCLE IS REDUCED FOLLOWING BLOCKADEOF ATP-SENSITIVE POTASSIUM CHANNELS

This study was designed to determine the role of ATP-sensitive potassi um channels in the control of the arteriolar diameter during functiona l hyperemia. The hamster cremaster muscle was prepared for in vivo mic roscopy and stimulated electrically for 1 min before and after topical application of 10 mu M glibenclamide to block ATP-sensitive potassium channels. Glibenclamide treatment resulted in a small, though not sig nificant, decrease in resting arteriolar diameter (P > 0.05). Glibencl amide almost completely inhibited the vasodilation of the first-order and the third-order arterioles in response to topical application of 1 mu M cromakalim (P < 0.05). During muscle stimulation, the first-orde r arterioles dilated from 69 +/- 3 to 89 +/- 3 mu m (n = 7), and the t hird-order arterioles dilated from 16 +/- 1 to 35 +/- 2 mu m (n = 7). In this set of experiments glibenclamide treatment resulted in a signi ficant decrease (similar to 4 mu m) in the resting diameters of the fi rst-order arterioles, but had no significant effect on the resting dia meter of third-order arterioles. Glibenclamide treatment significantly attenuated the vasodilation associated with muscle contraction to 72 +/- 3 and to 21 +/- 3 mu m, respectively (P < 0.05). These results sug gest that ATP-sensitive potassium channels are an important mediator i n the vasodilatory response to muscle stimulation in the hamster crema ster muscle.