Spontaneous oscillation of tone of blood vessel called vasomotion cause vessel to flow blood which is an oscillation of flow into an organ. Microcirculation is sensitive to hypoxic condition and metabolism but mechanism of vasomotion is still poorly understood.Design and method:
Purpose: We studied involvement of metabolism-mediated regulation by intracellular ATP level of vasomotion in human gastric artery. Methods: Conventional contractile measuring system and Western blot were used.Results:
Circular muscle of human gastric artery produced sustained tonic contraction of 1.0 ± 0.19 g by 50 mM high K+ (n = 36). Pinacidil (10 μM), which is known to activatorof ATP-sensitive K+ (KATP) channel inhibited vasomotion completely in a reversible manner. Inhibition of vasomotion by activators of KATP channel recovered by glibenclamide. Diazoxide (300 μM), cromakalim (10 μM) nicorandil (10 μM) which is known to activate KATP channel also completely blocked vasomotion in a glibenclamide sensitive manner. Inhibitory effect of these openers of KATP channel on serotonin and norepinephrine-induced contraction were also recoded in a glibenclmide-sensitive manner. In human artery, glucose-free condition which is elated metabolic changes inhibited vasomotion and it was recovered by glibenclamide. Finally, molecular subtypes of KATP channel was defined by Western blot in human artery.Conclusions:
Vasomotion of human gastroepiploic artery was inhibited by activation of specific subtypes of KATP channel and alteration of metabolism.