A model of potassium ion efflux during exercise of skeletal muscle

1979 ◽  
Vol 236 (1) ◽  
pp. R83-R90 ◽  
Author(s):  
Y. Hazeyama ◽  
H. V. Sparks

Potassium (K+) is a vasoactive agent and is released from muscle cells during exercise. A simple diffusion model does not predict the time course of K+ efflux during exercise, which decreases as the exercise progresses. We constructed a mathematical model using the concept of an active Na+-K+ ion pump to account for the decreased efflux during and uptake after exercise. Passive fluxes are calculated by the Nernst equation. Active fluxes are constrained to balance these passive fluxes at rest. The pump activity increases as either extracellular K+ or intracellular Na+ concentration increases. To test the model, the venous K+ efflux profile was simulated for direct stimulation (4/s) of the anterior calf mus cles of dogs. The model simulated the K+ release during the stimulation period and [K+] undershoot after the stimulation. The active Na+-K+ ATPase transport concept used in the model was further tested by observing K+ efflux after administration of ouabain. Ouabain infusion decreased K+ uptake during exercise slightly and abolished [K+] undershoot after the stimulation. These experimental data were matched by the model only if a discontinuous effect of ouabain is assumed. This suggests that ouabain may more completely block the sensitivity of the pump to intracellular [Na+] than to extracellular [K+].

1974 ◽  
Vol 52 (4) ◽  
pp. 852-871 ◽  
Author(s):  
K. Krnjević ◽  
M. E. Morris

K+-selective microelectrodes were used to measure extracellular K+ activity (aK) in the neuraxis of cats under Dial. In resting conditions, aK is stable (in range 2.0–3.0 mM) but may vary systematically with electrode position. Anoxia causes a progressive rise in aK, but only after a delay of 2–3 min and a maximum is not reached even after 15 min. Movements of the electrode are associated with transient increases in aK, presumably caused by tissue trauma. In areas rich in afferent terminals, direct stimulation through a microelectrode causes a sharp increase in aK, whose time course is consistent with diffusion from an instantaneous spherical source. Smaller increases in aK are produced by stimulating afferent fibers more peripherally, but definite changes can be recorded even with single pulses, and there is a cumulative, maintained rise in aK during repetitive stimulation at rates > 0.5 s−1. Although the observed changes in aK fit reasonably a simple diffusion model at low frequencies (< 5 s−1), a reuptake term (proportional to the change in aK) is necessary to obtain a satisfactory fit over a wide range of frequencies (1–200 s−1). The maximum aK reached during repetitive stimulation does not increase linearly with frequency, owing to a corresponding falling-off in K+ release per impulse.


1995 ◽  
Vol 269 (1) ◽  
pp. C217-C225 ◽  
Author(s):  
R. J. Sargeant ◽  
Z. Liu ◽  
A. Klip

The Na(+)-K(+)-ATPase presents several different isoforms of its alpha- and beta-subunits. We detected alpha 1- and beta 1-mRNA transcripts and polypeptides in 3T3-L1 fibroblasts; during differentiation into adipocytes, alpha 1-mRNA decreased, alpha 2-mRNA was induced, beta 1-mRNA dropped to undetectable levels, and beta 2-mRNA was never expressed, suggesting that 3T3-L1 adipocytes may express an unidentified Na(+)-K(+)-ATPase beta-subunit isoform. Insulin rapidly increased ion pump activity [ouabain-sensitive 86Rb+(K+) uptake] in 3T3-L1 fibroblasts and adipocytes without changing the plasma membrane concentration of alpha 1- or alpha 2-subunits as determined by subcellular membrane fractionation and immunoblotting or by [3H]ouabain binding to intact cells. Monensin, which raises the concentration of intracellular Na+, increased Na(+)-K+ pump activity, and no further stimulation was achieved with insulin. The stimulation of the pump by insulin was reduced by bumetanide, an inhibitor of the Na(+)-K(+)-2Cl- cotransporter, and was prevented by omission of extracellular Cl-. Insulin increased both ouabain-sensitive and bumetanide-sensitive 86Rb+(K+) uptake. These results suggest that insulin activation of the Na(+)-K(+)-ATPase in 3T3-L1 adipocytes is mediated by an elevation in intracellular Na+ that is likely the consequence of Na(+)-K(+)-2Cl- cotransporter activation.


1981 ◽  
Vol 59 (9) ◽  
pp. 1022-1025 ◽  
Author(s):  
M. E. Morris ◽  
K. Krnjević

Ca2+-sensitive microelectrodes, attached to CaCl2-containing micropipettes, were inserted into the dorsal hippocampus of rats under urethane. When Ca2+ was released iontophoretically, the amplitude and time course of the resultant increase in extracellular Ca2+ concentration could be fitted to a simple diffusion model, but the apparent diffusion coefficient of Ca2+ was only about 1/100 of its value in water, possibly because of reversible Ca2+ binding to hippocampal tissue. A further anomaly was a very low transport number (<0.01) for the release of Ca2+ from microelectrodes in vivo.


1989 ◽  
Vol 144 (1) ◽  
pp. 185-198 ◽  
Author(s):  
STEFAN SCHUSTER

The swimbladder volume and air volume within the breathing chambers of the anabantoid fish Colisa lalia have been measured. These data help in the understanding of some of the functions of these organs and are necessary for an analysis of their role in hearing and sound production. By means of a simple trick (based on new data) it was possible to analyse the time course of air volume changes in the breathing chambers at different temperatures. The results are well described by a simple diffusion model. The temperature-dependence of the time course suggests an interesting increase of the diffusion constant with temperature. Under constant conditions the chambers were always filled with about the same volume of air. No excess pressure was found. Typical values of a single chamber's air content range from 34 to 58μl. Air content increases with about the third power of fish length. By using the present data, the time course of air volumechanges in the chambers of a given fish can be estimated. Swimbladder volumes, determined using Boyle's law, ranged from 70 to 220μl and were also found to increase with about the third power of fish length, in accordance with a simple estimation. The data are discussed in relation to buoyancy, diffusion processes, blood circulation, hearing and sound production and suggest some interesting new work.


1996 ◽  
Vol 270 (4) ◽  
pp. G619-G633 ◽  
Author(s):  
M. Hocker ◽  
Z. Zhang ◽  
D. A. Fenstermacher ◽  
S. Tagerud ◽  
M. Chulak ◽  
...  

The enzyme L-histidine decarboxylase (HDC; EC 4.1.1.22), which converts L-histidine to histamine, plays a key role in the regulation of acid secretion. In the rat and human stomach, the peptide hormone gastrin appears to be one of the main regulators of HDC expression. In rats, marked elevation of gastric HDC mRNA abundance was observed within 12 h after induction of hypergastrinemia by a single injection of the proton-pump blocker omeprazole. In situ hybridization revealed that HDC expression occurred in the basal third of gastric glands where enterochromaffin-like cells are localized. To study the regulation of HDC gene transcription, 1,291 nucleotides of the 5'-flanking region of the rat HDC gene and the noncoding portion of exon 1 were cloned and sequenced. Gastrin and cholecystokinin (CCK) octapeptide equipotently stimulated the transcriptional activity of the rat HDC promoter three- to fourfold, and deletion analysis revealed the presence of a gastrin response element within 201 nucleotides upstream of the translational start site. Time-course studies revealed maximal activation of the HDC promoter after 12-36 h. Direct stimulation of protein kinase C (PKC) with the phorbol ester phorbol 12-myristate 13-acetate (PMA) substantially elevated rat HDC promoter activity, whereas induction of Ca2+ -dependent signaling pathways with thapsigargin was without effect. Downregulation or blockade of PKC abolished the effects of gastrin and PMA on the HDC promoter. These data indicate that stimulation of the CCK-B/gastrin receptor activates the rat HDC promoter in a time- and dose-dependent fashion and that this effect is primarily mediated via a PKC-dependent signaling pathway. Use of HDC as a model gene will allow further investigation of the intracellular pathways that are involved in gastrin-dependent gene regulation.


2019 ◽  
Author(s):  
Udo Boehm ◽  
Maarten Marsman ◽  
Han van der Maas ◽  
Gunter Maris

The emergence of computer-based assessments has made response times, in addition to response accuracies, available as a source of information about test takers’ latent abilities. The predominant approach to jointly account for response times and accuracies are statistical models. Substantive approaches such as the diffusion model, on the other hand, have been slow to gain traction due to their unwieldy functional form. In the present work we show how a single simplifying assumption yields a highly tractable diffusion model. This simple diffusion model is straightforward to analyse using Gibbs sampling and can be readily extended with a latent regression framework. We demonstrate the superior computational efficiency of our model compared to the standard diffusion model in a simulation study and showcase the theoretical merit of our model in an example application.


2008 ◽  
Vol 273-276 ◽  
pp. 500-505
Author(s):  
Gabriel Plascencia ◽  
David Jaramillo ◽  
Felipe Hernández ◽  
Jorge Luis González

Hydrogen embrittlement is a common problem for the integrity of oil conducting pipes. In this work, we estimate the rate of hydrogen penetration into an API 5L steel pipe welded by electric arc. The hydrogen penetration was estimated by means of data taken from ultrasonic measurements. As expected, the steel pipe becomes more brittle as the hydrogen penetration rate does so. A simple diffusion model was developed. The model confirms the strong dependency between the rate of penetration and the mechanical damage to the material.


1993 ◽  
Vol 185 (1) ◽  
pp. 305-323 ◽  
Author(s):  
J. H. Spring ◽  
S. A. Albarwani

1. We describe an in vitro perfused preparation of Acheta domesticus rectum which allows direct comparison of Malpighian tubule secretion and rectal absorption under identical conditions. Rectal absorption is stimulated four- to sixfold by corpora cardiaca (CC) homogenates and the stimulated rate is sufficiently rapid to account for all the fluid secreted by the tubules. 2. The time course for increased fluid absorption is similar to that required to stimulate electrogenic chloride transport in locusts and grasshoppers. Chloride is rapidly absorbed by the rectum under all conditions, along with lesser amounts of Na+ and K+. Unlike the situation in locusts, K+ uptake is unaffected by CC homogenates and the stimulated absorbate is NaCl-rich, similar in composition to the NaCl-rich tubule fluid produced under stimulated conditions. The absorbate is always slightly hypo-osmotic to the perfusate, reaching a maximum differential of approximately 15 mosmol l-1 following CC stimulation. 3. The antidiuretic factor that reduces tubule secretion does not promote fluid reabsorption by the rectum.


1995 ◽  
Vol 269 (1) ◽  
pp. R113-R123 ◽  
Author(s):  
D. Mutolo ◽  
F. Bongianni ◽  
M. Corda ◽  
G. A. Fontana ◽  
T. Pantaleo

Poststimulatory depression in respiratory activity induced by superior laryngeal nerve (SLN) stimulation was quantitatively investigated in 20 adult cats. The role played in this phenomenon by endogenous opioids was studied using the opiate antagonist naloxone. The effects of hypercapnia on the same phenomenon were also investigated for comparison. Experiments were performed on cats anesthetized with pentobarbitone or alpha-chloralose, vagotomized, paralyzed, and artificially ventilated with 100% O2. Some animals were also carotid sinus denervated. Respiratory output was monitored as integrated phrenic nerve activity. SLN stimulation produced apnea, which outlasted the stimulation period; when respiration resumed, it was markedly depressed as revealed mainly by a decrease in phrenic minute output, respiratory frequency, and rate of rise of inspiratory activity. Phrenic output recovered gradually to control levels following an exponential time course. These effects varied as a function of the duration of SLN stimulation. Naloxone administration (0.8 mg/kg iv) significantly reduced the duration of poststimulatory apnea and attenuated the depression of phrenic minute output of the first recovery breath as a result of changes in peak phrenic activity; it also accelerated the time course of recovery. Hypercapnia did not affect the duration of poststimulatory apnea, but attenuated the initial poststimulatory depression because of changes in respiratory frequency; the rate of recovery was reduced. The results provide characterization of poststimulatory respiratory depression of laryngeal origin in the adult cat and suggest a role of endogenous opioids in its genesis or modulation.


2020 ◽  
Vol 117 (15) ◽  
pp. 8611-8615 ◽  
Author(s):  
Rosa Anna M. Marino ◽  
Ross A. McDevitt ◽  
Stephanie C. Gantz ◽  
Hui Shen ◽  
Marco Pignatelli ◽  
...  

Electrical or optogenetic stimulation of lateral hypothalamic (LH) GABA neurons induces rapid vigorous eating in sated animals. The dopamine system has been implicated in the regulation of feeding. Previous work has suggested that a subset of LH GABA neurons projects to the ventral tegmental area (VTA) and targets GABA neurons, inhibiting them and thereby disinhibiting dopaminergic activity and release. Furthermore, stimulation-induced eating is attenuated by dopamine lesions or receptor antagonists. Here we explored the involvement of dopamine in LH stimulation-induced eating. LH stimulation caused sated mice to pick up pellets of standard chow with latencies that varied based on stimulation intensity; once food was picked up, animals ate for the remainder of the 60-s stimulation period. However, lesion of VTA GABA neurons failed to disrupt this effect. Moreover, direct stimulation of VTA or substantia nigra dopamine cell bodies failed to induce food approach or eating. Looking further, we found that some LH GABA fibers pass through the VTA to more caudal sites, where they synapse onto neurons near the locus coeruleus (LC). Similar eating was induced by stimulation of LH GABA terminals or GABA cell bodies in this peri-LC region. Lesion of peri-LC GABA neurons blocked LH stimulation-induced eating, establishing them as a critical downstream circuit element for LH neurons. Surprisingly, lesions did not alter body weight, suggesting that this system is not involved in the hunger or satiety mechanisms that govern normal feeding. Thus, we present a characterization of brain circuitry that may promote overeating and contribute to obesity.


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