Potassium inhibits nitric oxide and adenosine arteriolar vasodilatation via KIR and Na+/K+ATPase: implications for redundancy in active hyperaemia

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp6866-list-0001">Multiple vasodilators have been identified as being important in matching blood flow to the metabolism of contracting skeletal muscle and it has been hypothesized that this process is governed by redundancy between vasodilators, where one vasodilator can compensate for the loss of another.In the present study, we aimed to determine whether redundancy between vasodilators exists by investigating whether vasodilators relevant to skeletal muscle contraction can inhibit the effects of other vasodilators.We show that potassium can inhibit vasodilatations induced by adenosine and nitric oxide, and also that adenosine and nitric oxide can interact in a way that changes over time.Furthermore, we show that inward rectifying potassium channels and Na⁺/K⁺ATPase are partially mechanistically responsible for the interaction between potassium and adenosine and nitric oxide.Our data provide proof of principle that vasodilators relevant to muscle contraction interact and also that redundancy may govern the processes of active hyperaemia.