K+ potentiates hyperosmolarity-induced vasorelaxations in rat skeletal muscle arterioles.

Several regulatory mechanisms have been proposed for the exercise hyperemia in skeletal muscles. Since different vasoactive factors might interact during the hyperemic response, we investigated the influence of elevated K(+) concentrations on hyperosmolarity (HO)-induced vasorelaxations. Small gluteal rat arteries were isolated and mounted in an organ bath for isometric tension recording. After precontraction with norepinephrine, 20 (S20), 40 (S40) or 60 mM (S60) sucrose was added in control conditions (5 mM K(+); K5) or in the presence of additional 3 (K8) or 5 mM (K10) K(+). Removal of the endothelium and the addition of ouabain, Ba(2+), iberiotoxin or 18-alpha glycyrrhetinic acid (alphaGA) were used to study the underlying mechanisms. Sucrose evoked significant concentration-dependent vasorelaxations (S20 15.62+/-1.61%; S40 26.47+/-1.71%; S60 43.66+/-2.50%), which were significantly increased on addition of 3 and 5 mM. After removal of the endothelium and in the presence of 5 x 10(-5) M alphaGA, the influence of K(+) was significantly blocked but not in the presence of 5 x 10(-5) M ouabain. The K(IR) channel inhibitor Ba(2+) and BK(Ca) channel inhibitor iberiotoxin totally abolished the potentiating effect. We conclude that K(+) significantly enhances the relaxing effect of HO in gluteal blood vessels. We hypothesize that K(+) may stimulate the endothelial K(IR) channels which elicits the release of a mediator of the BK(Ca) channels. This factor may be transferred through myo-endothelial gap-junctions to the smooth muscle cells where modulation of the BK(Ca) channels sensitizes the arteries for hyperosmolarity-induced relaxations.

The measurement of competitive anxiety during balance beam performance in gymnasts.

The purpose of the present study was to investigate competitive anxiety during balance beam performance in gymnasts. Competitive anxiety was assessed continuously by heart rate monitoring and by retrospective self-report of nervousness in eight female national level gymnasts during their balance beam routine during one competition and two training sessions. A significant negative correlation was found between the score of the retrospective self-report of nervousness and performance during the routine. There were no significant differences in performance score by the judges between the three test sessions. There were also no differences in the retrospective self-report of nervousness. However, heart rate was significantly higher during the competition session than during the training sessions. The potential value of the retrospective report of nervousness for the study of critical events during gymnastic performance is illustrated. The results are discussed in the light of catastrophe theory.

Hyperosmolarity causes BK Ca-dependent vasodilatations in rat skeletal muscle arteries.

PURPOSE: The release of different metabolites during skeletal muscle contraction causes a pronounced increase in extracellular osmolarity (hyperosmolarity (HO)). HO has been considered as a possible mediator of the exercise hyperemia. In the present study, we investigated the vasodilatory effect of physiologically relevant increases in the extracellular osmolarity in isolated rat gluteal muscle arterioles. In addition, we analyzed the underlying mechanisms of the HO-induced vasodilatations. METHODS: Rat gluteal arteries were isolated and mounted in an organ bath for isometric tension recording. After precontraction with norepinephrine, 20, 40, or 60 mmol x L(-1) sucrose, mannitol, or urea was added in control conditions, after removal of the endothelium or in the presence of inhibitors. RESULTS: Application of sucrose or mannitol induced large and fast concentration-dependent vasodilatations (up to 46.15% with 60 mmol x L(-1) sucrose). Removal of the vascular endothelium had no effect on this relaxation. Inhibition of the Na+/K+ pumps with ouabain, the Kir IR channels with Ba2+ and the K ATP channels with glibenclamide did not alter the HO-induced relaxations. Incubation with the KCa channel blockers charybdotoxin and apamin significantly inhibited sucrose-induced vasodilatations. In addition, application of the specific BK Ca channel blocker iberiotoxin significantly decreased the HO-induced vasodilatations. CONCLUSION: The present study shows that an increase in the extracellular osmolarity elicits strong, fast, and long-lasting relaxations of rat skeletal muscle arterioles, suggesting an important role both at the onset and during the steady-state phase of an exercise bout. Vascular smooth muscle BK Ca channels seem to play a crucial role in the HO-induced vasorelaxations.

Hyperosmolarity increases K+-induced vasodilations in rat skeletal muscle arterioles.

PURPOSE: Exercise hyperemia is mediated by a multitude of vasoactive metabolites released from the active skeletal muscle. Because several vasoactive factors might interact during the hyperemia response, we investigated the influence of hyperosmolarity (HO) on K(+)-induced relaxations. METHODS: Small gluteal rat arteries (diameter: 245 +/- 6 microm) were isolated and mounted in an organ bath for isometric tension recording. After precontraction with norepinephrine, 1, 2, or 3 mM K(+) was added in both control, moderate, or high hyperosmotic (30 mM (S30) or 60 mM sucrose (S60)) conditions. Endothelial removal and the addition of ouabain, Ba(2+), 5-nitro-2-(3-phenyl-propylamino) benzoic acid (NPPB), or glibenclamide was used to study the underlying mechanisms. RESULTS: The K(+)-induced relaxations were significantly (P < 0.001) increased in the presence of S30 and S60. Endothelial removal and the addition of glibenclamide or ouabain did not reduce the HO-induced increased sensitivity to K(+). The application of Ba abolished the influence of HO on the K(+)-induced relaxations. NPPB, a volume regulated anion channel (VRAC) blocker, mimicked the influence of HO by significantly (P < 0.05) increasing the K(+)-induced relaxations. Remarkably, the application of Ba(2+) abolished the sensitizing effect of NPPB on K(+)-induced relaxations. CONCLUSION: HO increases the sensitivity of the rat gluteal skeletal muscle arteries to the vasodilating effect of K(+). It is hypothesized that HO inhibits VRAC causing smooth muscle hyperpolarization. This possibly sensitizes the K(ir)-channels that are known to be involved in the K-induced relaxations in this type of arteries.

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 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. 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.