title: Exercise training increases inwardly rectifying K(+) current and augments K(+)-mediated vasodilatation in deep femoral artery of rats.
abstract: OBJECTIVE
  A moderate increase in extracellular [K(+)] ([K(+)](e)) induces relaxation of small arteries by activating inwardly rectifying K(+) current (I(Kir)). The K(+)-induced vasodilatation is an important mechanism for exercise-induced hyperaemia in skeletal muscle. We investigated whether I(Kir) and K(+)-induced vasodilatation are enhanced in deep femoral arteries (DFAs) from exercise-trained rats (ET rats; treadmill running for 20 min at 20 m/min, 3 days/week for 2 weeks). The effects of exercise training on K(+)-induced vasodilatation and I(Kir) were also investigated in cerebral (CA) and mesenteric arteries.
  
  
  RESULTS
  The K(+)-induced vasodilatation of DFAs and the density of I(Kir) and voltage-gated K(+) current (I(Kv)) were increased in DFA myocytes of ET rats. The myogenic tone of the DFA was unchanged by exercise. Although similar functional up-regulations of I(Kir) and I(Kv) were observed in CA myocytes, the K(+)-induced vasodilatation was not increased in the CA of ET rats. Interestingly, concomitant to the increases in I(Kir) and I(Kv), background Na(+) conductance was also increased in the CA myocytes. However, such an effect was not observed in DFA myocytes from ET rats. Neither I(Kir) nor K(+)-induced vasodilatation was observed in mesenteric arteries of ET rats.
  
  
  CONCLUSIONS
  The present study provides evidence that regular exercise up-regulates I(Kir) in DFA and CA myocytes. Although the increase in I(Kir) was observed in two types of arteries, augmentation of K(+)-induced relaxation was observed only in the DFA of ET rats, possibly due to the increased Na(+) conductance in CA myocytes. The increases in I(Kir) and K(+)-induced vasodilatation of the arteries of skeletal muscle suggest novel mechanisms of improved exercise hyperaemia with physical training.
authors.affiliation: Department of Physiology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, Seoul 110-799, Korea.
authors.forename: Chun Zi
authors.initials: CZ
authors.lastname: Jin
authors.forename: Hyang Sun
authors.initials: HS
authors.lastname: Kim
authors.forename: Eun Yeong
authors.initials: EY
authors.lastname: Seo
authors.forename: Dong Hoon
authors.initials: DH
authors.lastname: Shin
authors.forename: Kyung Sun
authors.initials: KS
authors.lastname: Park
authors.forename: Yang-Sook
authors.initials: YS
authors.lastname: Chun
authors.forename: Yin Hua
authors.initials: YH
authors.lastname: Zhang
authors.forename: Sung Joon
authors.initials: SJ
authors.lastname: Kim
mesh_terms: D000818:Animals; D002536:Cerebral Arteries / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D005263:Femoral Artery / Q000378:metabolism* / Q000503:physiopathology; D006940:Hyperemia / Q000378:metabolism* / Q000503:physiopathology; D015640:Ion Channel Gating; D008297:Male; D008564:Membrane Potentials; D008638:Mesenteric Arteries / Q000378:metabolism / Q000503:physiopathology; D018715:Microscopy, Video; D018482:Muscle, Skeletal / Q000098:blood supply*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000503:physiopathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D005082:Physical Exertion; D011188:Potassium / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow; D012964:Sodium / Q000378:metabolism; D013152:Splanchnic Circulation; D013997:Time Factors; D015854:Up-Regulation; D014664:Vasodilation
chemical_list: D024661:Potassium Channels, Inwardly Rectifying; D012964:Sodium; D011188:Potassium