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Published on: March 15, 2019
K+ as a vasodilator in resting human muscle: implications for exercise hyperaemia
1Institute of Molecular Biology and Physiology, Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark. cjuel@aki.ku.dk
Potassium (K(+)) infusions at physiological levels increase leg blood flow (LBF) by causing vasodilation. This effect is mediated by Kir2.1 channels and suggests K(+) contributes to exercise hyperemia.
Area of Science:
- Physiology
- Cardiovascular Research
Background:
- Potassium (K(+)) released from contracting skeletal muscle is traditionally viewed as a vasodilator.
- This concept is largely based on studies using non-physiological K(+) concentrations.
Purpose of the Study:
- To investigate the precise role of K(+) in regulating blood flow.
- To determine if physiological K(+) levels induce vasodilation in resting skeletal muscle.
Main Methods:
- Leg blood flow (LBF) and arterio-venous O(2) difference were measured in 13 subjects.
- Graded infusions of K(+) were administered into the femoral artery.
- The effect of Ba(2+), a Kir2.1 channel inhibitor, on K(+)-induced vasodilation was assessed.
Main Results:
- Physiological K(+) infusions significantly increased LBF and decreased the arterio-venous O(2) difference, indicating vasodilation.
- The vasodilatory effect of K(+) was completely blocked by Ba(2+) inhibition of Kir2.1 channels.
- The combined effect of ATP and K(+) on LBF was additive.
Conclusions:
- Physiological K(+) levels induce vasodilation in resting skeletal muscle via Kir2.1 channels.
- K(+) released during muscle contraction likely contributes to exercise-induced hyperemia.
- However, K(+) alone may only account for a small portion of the overall exercise hyperemic response.
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