Work-induced potassium changes in skeletal muscle and effluent venous blood assessed by liquid ion-exchanger microelectrodes

Hník, P; Holas, M; Krekule, I; Kŭriz, N; Mejsnar, J; Smiesko, V; Ujec, E; Vyskočil, F.

doi:10.1007/bf00588685

Cited by 128 publications

(72 citation statements)

References 32 publications

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“…49), but the release may not be linearly related to stimulus frequency over multiple stimuli (25,26). We show that K ϩ involvement does not increase as stimulus frequency increases over 2 min.…”

Section: How Stimulation Parameters May Affect the Vasodilator Complementioning

confidence: 68%

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Dua¹,

Dua²,

Murrant³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Dua AK, Dua N, Murrant CL. Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency. Am J Physiol Heart Circ Physiol 297: H433-H442, 2009. First published May 22, 2009 doi:10.1152/ajpheart.00216.2009.-To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated four to five skeletal muscle fibers in the anesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibers. Diameter was measured before, during, and after 2 min of skeletal muscle contraction stimulated over a range of stimulus frequencies [4,20, and 40 Hz;15 . L-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60 cpm. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40 Hz. Glibenclamide inhibited all dilations at all stimulus and contraction frequencies, and DAP did not inhibit dilations at any stimulus frequencies while attenuating dilation at a contraction frequency of 60 cpm only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency; therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia. stimulus frequency; contraction frequency; arteriole; skeletal muscle contraction; active hyperemia BLOOD FLOW TO ACTIVE SKELETAL muscle increases during contraction. It is hypothesized that active skeletal muscle cell metabolites are a source of vasodilators that cause active hyperemia during contraction, but there is little consensus as to the identity of the vasodilators involved. A host of potential metabolic vasodilators such as adenosine (ADO), hydrogen ions, decreased oxygen tension, carbon dioxide, phosphate, etc., as well as a host of endothelial-derived products and products of muscle activation such as nitric oxide (NO), potassium (K ϩ ), prostaglandins, ACh, ATP-dependent K ϩ (K ATP ) channels, etc. (for review, see Refs. 6,18,28,36), have been implicated in the processes of active hyperemia, but there is a general lack of agreement as to the relative importance of each. We have been investigating the impact of stimulation parameters in the processes of arteriolar vasodilation during active hyperemia to understand this general lack of agreement. We surmised that if the dilators are proposed to be products of skeletal muscle activation or metabolism then it stands to reason that if activation or metabolism is changed through different stimulation parameters then the dilators being produced may also change. Thus, to understand the impact that stimulation parameters have on the production of different vasodilators in active hyperemia, we have investigated the effects of stimulation par...

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Section: How Stimulation Parameters May Affect the Vasodilator Complementioning

confidence: 68%

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Dua¹,

Dua²,

Murrant³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Adrian and Peachey (46) calculate that a single action potential alters the luminal potassium concentration by about ϩ0.3 mM. Moreover, the extracellular potassium concentration elevated physiologically to 8 -9 mM in the vicinity of stimulated skeletal muscles, causing hyperkalemic periodic paralysis (47). The potassium accumulation in the lumen of the transverse tubules can only be dissipated relatively slowly by diffusion out of the mouth of the transverse tubules and by active pumping back into the myoplasm across the transverse tubule wall.…”

Section: Effect Of Intracellular Ca 2ϩ and Pkc On Irk1 Expressionmentioning

confidence: 99%

Opposite Effect of Intracellular Ca2+ and Protein Kinase C on the Expression of Inwardly Rectifying K+Channel 1 in Mouse Skeletal Muscle

Shin

Park

Kwon

et al. 1997

Journal of Biological Chemistry

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The level of inwardly rectifying K ؉ channel 1 (IRK1) mRNA decreased upon denervation and increased during muscle differentiation in mouse skeletal muscle. To identify the mechanism(s) underlying the regulation of IRK1 mRNA expression, we examined its expression using the well differentiated C2C12 mouse skeletal muscle cell line as a model system. Since nerve-induced muscle activity results in contraction, it was questioned whether the changes in IRK1 expression might be relevant to the increased intracellular calcium that functions as a cytoplasmic messenger in excitation-contraction coupling. Indeed, activation of either L-type calcium channels or ryanodine receptors increased the level of IRK1 mRNA. More directly, ionomycin activated the IRK1 expression in time-and dose-dependent manners, which was abolished by treatment with EGTA. Genistein, a tyrosine kinase inhibitor, also abolished the stimulating effect of ionomycin. Meanwhile, activation of protein kinase C by 12-O-tetradecanoylphorbol acetate (TPA) markedly decreased the level of IRK1 mRNA, which required ongoing protein synthesis. Actinomycin D experiments revealed that ionomycin increased the half-life of IRK1 mRNA from 0.86 to 1.97 h, but TPA decreased it to 0.38 h. However, neither ionomycin nor TPA appreciably altered the rate of IRK1 gene transcription. Based on these observations, we conclude that intracellular calcium and protein kinase C are oppositely involved in the muscle activity-dependent regulation of IRK1 gene expression and that both act at the level of mRNA stability.It has been known that denervation influences many biophysical and biochemical properties of skeletal muscle fibers (1-7). The mechanisms by which denervation initiates these changes are still unclear. They may be caused by the loss of neurotrophic factors normally released from the nerve terminals (8, 9). Alternatively, the electrical inactivity of the denervated muscle might be responsible, since direct electrical stimulation to the denervated muscle restores all passive electrical parameters of the membrane that were observed without denervation (10, 11). Considering the importance of calcium in the process of muscle contraction induced by neural activity, calcium may play a critical role in linking the biochemical and biophysical changes with muscle activity.Calcium is known to be involved in many cellular events as a second messenger. A regulatory role of calcium in the expression of sodium channels, acetylcholinesterase, and nicotinic acetylcholine receptor has been suggested (12-16). In addition, it has recently been shown that calcium influx blocks the expression of nicotinic acetylcholine receptor ␣-subunit gene in chick skeletal muscle (17). There are reports that coupling of the electrical activity with altered gene expression is mediated by protein kinase C (PKC) 1 pathway (18, 19). Gonoi and Hasegawa (20) demonstrate by using a patch clamp method that innervation of skeletal muscle fibers plays a key role in the induction and maintenance of inwardly rectifyin...

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“…There is a net and large potassium efflux during fatigue which is well documented (Lucier & Mainwood, 1972;Hnik et al 1976;Hirsche, Schumaker & Hagemann, 1980;Sj0gaard, Adams & Saltin, 1985). The accumulation of K+ at the surface and in T-tubules is believed to depolarize the sarcolemma and lead to a failure of excitation-contraction coupling resulting in an impairment of force production (Sj0gaard et al 1985;Sj0gaard, 1990Sj0gaard, , 1991Renaud & Light, 1992).…”

mentioning

confidence: 97%

The effect of glibenclamide on frog skeletal muscle: evidence for K+ATP channel activation during fatigue.

Light

Comtois

Renaud

1994

The Journal of Physiology

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1. The purpose of this study was to determine whether ATP-sensitive K+ (KATP) channels are activated and contribute to the decrease in force during fatigue development in the sartorius muscle of the frog, Rana pipiens. Tetanic force (elicited by field stimulation), action potential and membrane conductance (using conventional microelectrodes), were measured in the presence and absence of glibenclamide, a KATP channel antagonist. Experiments were performed in bicarbonate-buffered solutions at pH 7-2.2. In unfatigued muscle 100 ,umol I-' glibenclamide had no effect on the resting potential, the overshoot, the half-depolarization time or the maximum rate of depolarization of action potentials, while the mean half-repolarization time increased by 19 ± 4 % (± S.E.M.) and the maximum rate of repolarization decreased by 17 + 5 %. 3. Fatigue was elicited using 100 ms tetanic contractions every I s for 3 min. In the absence of glibenclamide the mean half-repolarization time increased from 057 + 005 to 089 + 0 05 ms during fatigue. The mean half-repolarization times after fatigue, when muscle fibres were exposed to 100 ,umol I1 glibenclamide either 60 min prior to fatigue or 60 s before the end of fatigue, were 1-16 + 0-08 and 1t17 + 0 07 ms respectively.Application of 100 #smol I-' glibenclamide after 5 min of recovery did not increase the half-repolarization time, but decreased the rate of recovery compared to control values.4. In unfatigued muscles, 100 jumol I' glibenclamide did not affect the tetanic contraction. In the absence of glibenclamide, the mean tetanic force after fatigue was 11 0 + 0 9 % of prefatigue values. Application of 100 umol I' glibenclamide 60 min before fatigue increased the rate of fatigue development as the mean tetanic force was 4-8 + 0-8 % after 3 min of stimulation. The addition of 100 ,umol I-' glibenclamide 60 s before the end of fatigue had no effect on tetanic force during this time compared to control. 5. In the absence of glibenclamide, muscles recovered 90-1 + 1-6 % of their tetanic force after 100 min. Addition of 100,umol I' glibenclamide 60 min prior to fatigue significantly reduced the capacity of muscles to recover their tetanic force: after 100 min of recovery tetanic force was only 47-3 + 9.4 % of the pre-fatigue value. Application of 100 jumol I' glibenclamide 60 s prior to the end of fatigue had a much smaller effect on the recovery as 79.4 + 6'2 % of the tetanic force was recovered in 100 min. Addition of glibenclamide after 5 min of recovery had no effect. 6. The results from this study support the proposal that KATP channels are activated during fatigue and they contribute to the repolarization phase of the action potential. Although no evidence was found that activation of KATP channels during fatigue contributes to the force decrease during fatigue development, the impairment of force recovery following fatigue in the presence of glibenclamide supports the notion that KATP channels play an important protective role.

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Work-induced potassium changes in skeletal muscle and effluent venous blood assessed by liquid ion-exchanger microelectrodes

Cited by 128 publications

References 32 publications

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Opposite Effect of Intracellular Ca2+ and Protein Kinase C on the Expression of Inwardly Rectifying K+Channel 1 in Mouse Skeletal Muscle

The effect of glibenclamide on frog skeletal muscle: evidence for K+ATP channel activation during fatigue.

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