Exercise training increases inwardly rectifying K(+) current and augments K(+)-mediated vasodilatation in deep femoral artery of rats

AIMS: 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.

METHODS AND 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.

CONCLUSION: 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.