Functional hyperemia in striated muscle is reduced following blockade of ATP-sensitive potassium channels.
This study was designed to determine the role of ATP-sensitive potassium channels in the control of the arteriolar diameter during functional hyperemia. The hamster cremaster muscle was prepared for in vivo microscopy and stimulated electrically for 1 min before and after topical application of 10 microM glibenclamide to block ATP-sensitive potassium channels. Glibenclamide treatment resulted in a small, though not significant, decrease in resting arteriolar diameter (P > 0.05). Glibenclamide almost completely inhibited the vasodilation of the first-order and the third-order arterioles in response to topical application of 1 microM cromakalim (P < 0.05). During muscle stimulation, the first-order arterioles dilated from 69 +/- 3 to 89 +/- 3 microns (n = 7), and the third-order arterioles dilated from 16 +/- 1 to 35 +/- 2 microns (n = 7). In this set of experiments glibenclamide treatment resulted in a significant decrease (approximately 4 microns) in the resting diameters of the first-order arterioles, but had no significant effect on the resting diameter of third-order arterioles. Glibenclamide treatment significantly attenuated the vasodilation associated with muscle contraction to 72 +/- 3 and to 21 +/- 3 microns, respectively (P < 0.05). These results suggests that ATP-sensitive potassium channels are an important mediator in the vasodilatory response to muscle stimulation in the hamster cremaster muscle.
Saito
Y
Y
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA.
McKay
M
M
Eraslan
A
A
Hester
R L
RL
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001160:Arterioles / Q000187:drug effects; D006224:Cricetinae; D004558:Electric Stimulation; D005905:Glyburide / Q000494:pharmacology; D006940:Hyperemia / Q000209:etiology*; D008297:Male; D008647:Mesocricetus; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000378:metabolism; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D026902:Potassium Channel Blockers; D015221:Potassium Channels; D000255:Adenosine Triphosphate; D005905:Glyburide