Potassium potently relaxes small rat skeletal muscle arteries

Introduction: Skeletal muscle contraction elicits an explosive rise in interstitial potassium (K+) concentration. K+ has been considered as one of the most potent vasoactive metabolites in skeletal muscle arterioles. Studies on isolated blood vessels report large relaxations when extracellular [K+] is increased up to 10 mM. We studied the effects of smaller and physiologically more relevant increases in [K+] (adding 1, 2, and 3 mM) and compared them with relaxations induced by the endothelium derived hyperpolarizing factor (EDHF). Methods: Rat gluteal arteries were isolated and mounted in an organ bath for isometric tension recording. After precontraction with norepinephrine, acetylcholine or K+ was added in control conditions, after removal of the endothelium or in the presence of ouabain or Ba2+. Results: Application of 1, 2, or 3 mM K+ induced large vasodilatations (up to 75.4% with 3 mM) (N = 40), which were more sustained at the higher concentrations. Removal of the vascular endothelium had no effect on this relaxation. Inhibition of the K-ir channels with Ba2+ did not alter the K+-induced relaxations, although it significantly inhibited the EDHF-mediated relaxation. Incubation with ouabain significantly decreased the K+- and EDHF-induced relaxation. Simultaneous application of Ba2+ and ouabain totally abolished both K+- and EDHF-induced responses. Conclusion: Even small increases in extracellular K+ concentration elicit large endothelium-independent and ouabain-sensitive relaxations in small skeletal muscle arteries. The fact that both K+- and EDHF-induced vasorelaxations show similar characteristics indicates that K+ might be the EDHF in this type of artery.