Sympatholytic effect of intravascular ATP is independent of nitric oxide prostaglandins Na+/K+‐ATPase and KIR channels in humans

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12466-list-0001">Intravascular ATP attenuates sympathetic vasoconstriction (sympatholysis) similar to what is observed in contracting skeletal muscle of humans, and may be an important contributor to exercise hyperaemia.Similar to exercise, ATP‐mediated vasodilatation occurs via activation of inwardly rectifying potassium channels (KIR), and synthesis of nitric oxide (NO) and prostaglandins (PG).However, recent evidence suggests that these dilatatory pathways are not obligatory for sympatholysis during exercise; therefore, we tested the hypothesis that the ability of ATP to blunt α1‐adrenergic vasoconstriction in resting skeletal muscle would be independent of KIR, NO, PGs and Na⁺/K⁺‐ATPase activity.Blockade of KIR channels alone or in combination with NO, PGs and Na⁺/K⁺‐ATPase significantly reduced the vasodilatatory response to ATP, although intravascular ATP maintained the ability to attenuate α1‐adrenergic vasoconstriction.This study highlights similarities in the vascular response to ATP and exercise, and further supports a potential role of intravascular ATP in blood flow regulation during exercise in humans.