Potassium potently relaxes small rat skeletal muscle arteries

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).

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+.

Application of 1, 2, or 3 mM K+ induced large vasodilations (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 Kir 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.

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.