Juel C, Olsen S, Rentsch R L, González-Alonso J, Rosenmeier J B
Institute of Molecular Biology and Physiology, Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark.
Acta Physiol (Oxf). 2007 Aug;190(4):311-8. doi: 10.1111/j.1748-1716.2007.01678.x. Epub 2007 Mar 30.
Potassium (K(+)) released from contracting skeletal muscle is considered a vasodilatory agent. This concept is mainly based on experiments infusing non-physiological doses of K(+). The aim of the present study was to investigate the role of K(+) in blood flow regulation.
We measured leg blood flow (LBF) and arterio-venous (A-V) O(2) difference in 13 subjects while infusing K(+) into the femoral artery at a rate of 0.2, 0.4, 0.6 and 0.8 mmol min(-1).
The lowest dose increased the calculated femoral artery plasma K(+) concentration by approx.1 mmol L(-1). Graded K(+) infusions increased LBF from 0.39 +/- 0.06 to 0.56 +/- 0.13, 0.58 +/- 0.17, 0.61 +/- 0.11 and 0.71 +/- 0.17 L min(-1), respectively, whereas the leg A-V O(2) difference decreased from 74 +/- 9 to 60 +/- 12, 52 +/- 11, 53 +/- 9 and 45 +/- 7 mL L(-1), respectively (P < 0.05). Mean arterial pressure was unchanged, indicating that the increase in LBF was associated with vasodilatation. The effect of K(+) was totally inhibited by infusion (27 micromol min(-1)) of Ba(2+), an inhibitor of Kir2.1 channels. Simultaneous infusion of ATP and K(+) evoked an increase in LBF equalled to the sum of their effects.
Physiological infusions of K(+) induce significant increases in resting LBF, which are completely blunted by inhibition of the Kir2.1 channels. The present findings in resting skeletal muscle suggest that K(+) released from contracting muscle might be involved in exercise hyperaemia. However, the magnitude of increase in LBF observed with K(+) infusion suggests that K(+) only accounts for a limited fraction of the hyperaemic response to exercise.
收缩的骨骼肌释放的钾离子（K⁺）被认为是一种血管舒张剂。这一概念主要基于输注非生理剂量钾离子的实验。本研究的目的是探讨钾离子在血流调节中的作用。
我们在13名受试者中测量了腿部血流量（LBF）和动静脉（A-V）氧差，同时以0.2、0.4、0.6和0.8 mmol min⁻¹的速率向股动脉输注钾离子。
最低剂量使计算出的股动脉血浆钾离子浓度增加约1 mmol L⁻¹。分级输注钾离子使LBF分别从0.39±0.06增加到0.56±0.13、0.58±0.17、0.61±0.11和0.71±0.17 L min⁻¹，而腿部A-V氧差分别从74±9降至60±12、52±11、53±9和45±7 mL L⁻¹（P<0.05）。平均动脉压未改变，表明LBF的增加与血管舒张有关。钾离子的作用被Kir2.1通道抑制剂钡离子（27 μmol min⁻¹）的输注完全抑制。同时输注ATP和钾离子引起的LBF增加等于它们各自作用之和。
生理剂量的钾离子输注可使静息LBF显著增加，而抑制Kir2.1通道可完全消除这种增加。在静息骨骼肌中的当前发现表明，收缩肌肉释放的钾离子可能参与运动性充血。然而，钾离子输注时观察到的LBF增加幅度表明，钾离子仅占运动性充血反应的有限部分。
