Increase In Extracellular Potassium Concentration Research Articles

The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate

The course of ischemic increase of extracellular potassium concentration ([K+]e) was studied in rat cerebral cortex with potassium selective microelectrodes and correlated to the preischemic functional and metabolic state. Complete cerebral ischemia was induced in artificially ventilated rats by cardiac arrest. Seven different functional states including conditions with cerebral hypermetabolism (seizures, amphetamine intoxication, hyperthermia) and hypometabolism (barbiturate anesthesia, hypothermia) were chosen in order to cover a wide range of cerebral metabolic rates (CMRO2 : 28.7--2.4 ml O2/(100 g)/min). The ischemic increase of [K+]e was delayed in conditions with low CMRO2 and accelerated in conditions with high CMRO2; the time interval to the terminal steep rise in extracellular potassium concentration varied within the extremes of 35 +/- 5 and 365 +/- 12 sec (means +/- S.E.M.), the control state (N2O-analgesia) being 116 +/- 5 sec. In groups with high CMRO2 electrocortical activity ceased within 15 sec and in groups with low CMRO2 within 22 sec. The rates of the ischemic [K+]e increase, measured as rate of change in the potassium electrode potential (mV/sec), remained high in conditions with high preischemic CMRO2 and low in conditions with low CMRO2, indicating a remaining influence of the preischemic metabolism on membrane ion permeability. These results support previous metabolic data indicating that the rate of consumption of high energy phosphates during ischemia mirrors the preischemic cerebral metabolic rate. Phenobarbital anesthesia did not change the initial rate of [K+]e increase but reduced the rate of [K+]e increase later during ischemia, suggesting a special effect of barbiturates on partly depolarized membranes.

Studies on potassium transport through glial cell membranes (author's transl)

The retina of the honeybee drone is used as a model for the study of ion movements across the membranes of the glial cells caused by changes in the extracellular potassium concentration. The values found for changes in extracellular potential suggest that at least some of the potassium that enters glial cells in an active region of tissue is associated with an efflux of potassium from parts of the glial syncytium not affected by an increase in extracellular potassium concentration. In addition, it appears that ions other than K+ cross the glial membrane.

Mechanism of extracellular potassium stimulation of protein synthesis in the in vitro hippocampus.

AbstractTransverse slices of guinea‐pig hippocampus respond to small increases in extracellular potassium concentration [K +] by showing a marked augmentation in the rate of incorporation of labelled precursor amino acid into protein. We find that this augmentation is manifested equally in superfusing solutions containing low specific activity/high concentration precursor and high specific activity/low concentration precursor. This provides additional evidence that the effect of extracellular [K +] is on the rate of protein synthesis and not on the precursor pool. Extracellular [K +] augments amino acid incorporation normally in the presence of concentrations of α‐amanatin and actinomycin D which are inhibiting RNA synthesis by over 97%. This suggests the effect is exerted post‐transcriptionally. Extracellular [K +] causes an unattenuated increase in protein synthesis in the presence of high Mg2+ (20mm) or low Ca2+ (0 mm) in the superfusate–suggesting this effect of [K +] does not result from an effect on neurotransmitter release. Increases in extracellular [K+] which increase protein synthesis threefold (1.3‐6.4mm‐K +) increase the intracellular [K +]/[Na +] 2‐fold. 3 x 10‐7m‐Ouabain. which lowers incorporation by 40‐50% lowers [K +]/[Na +] by about 50% while having no effect on the uptake of labelled precursor or on the cell concentrations of ATP. These results suggest that protein synthesis in the cell is sensitive to [K. +]/[Na +] and that an alteration in this ratio is the mechanism by which the concentration of extracellular [K +] affects the rate of in vitro hippocampal protein synthesis. This effect of extracellular [K +] on synthesis is not observed in slices from non‐cerebral organs of the guinea pig.

Changes of extracellular potassium activity in isolated spinal cord of frog under high Mg 2+ concentration

Dorsal root potentials (DRPs) and changes of extracellular K + accompanying orthodromic stimulation were studied under high Mg 2+ concentration in isolated spinal cord of the frog. Under 20 mM MgSO 4 when synaptic transmission was blocked the amplitude of DRPs, evoked by a single volley in a dorsal root, decreased to 5–15% of the control and the transient increase of extracellular potassium concentration [K] e evoked by 100 Hz orthodromic stimulation decreased to 10–15%. It is suggested that the DRPs, resistant to high Mg 2+ concentration, are produced by transient increase of K + that leaks from primary afferents.

Anoxic changes of extracellular potassium concentration in the cerebral cortex of young rats

Changes of extracellular potassium concentration during terminal anoxic depolarization were studied in the cerebral cortex of 5-, 9-, 14-, and 19-day-old rats by means of K +-specific microelectrodes. Resting level was found to be the same (about 3 m m) in all age groups. Anesthetized rats were killed by an overdose of d-tubocurarine. An increase of extracellular potassium concentration starting immediately after respiratory arrest was divided into four phases according to the slope of the increase. Phase I was the slowest, phase III the fastest. Second and third phases started at [K +] e levels of 6.5 to 8.6 and 20 m m, respectively. Whereas the above transition levels between various phases did not change during ontogenesis, their slope increased with age; phase III started after 31.8, 14.5, 11.9, and 7.8 min in the 5-, 9-, 14-, and 19-day-old rats. Individual phases of extracellular potassium concentration increase could be ascribed to changes of membrane permeability. Slow K + release in young animals reflects their higher resistance against anoxia and developmental changes in the relative volume of extracellular space in the cerebral cortex. The maximal level of extracellular potassium reached during the 5-min period after phase III increased with age (52.6 m m in 5-day-old rats, 75.7 m m in 19-day-olds) in accordance with data on developmental changes of potassium of the brain.

The effect of synaptic activation on the extracellular potassium concentration in the hippocampal dentate area, in vitro

Excitatory synaptic inputs to the granule cells of the dentate area elicit first of all EPSPs and then action potentials in the cells, giving rise to the characteristic extracellular field potentials referred to as the synaptic wave and population spike 13. The excitability of the cell population is easily altered by prior conditioning shocks or trains of shocks 1-~,9,13, though the mechanisms of these alterations are not fully understood. It is possible that potassium (K +) etttux from the granule cells might account for some of the alterations in excitability. It is already known that large increases in extracellular potassium concentration can accompany states of abnormal cortical function such as spreading depression 7,1°,17 and epilepsy 6. In this study we have used K+-sensitive microelectrodes 18 to show that there are detectable changes in the K + concentration around the dentate granule cells of the guinea pig hippocampus after synaptic activation of a well defined afferent pathway. We are not at present able to say whether such changes in fact account for changes in excitability of the cell population. Slices from the ventral surface of the hippocampus of guinea-pig brains were cut approximately 500 #m thick and maintained at 20-23 °C in vitro, cut surface uppermost, at the surface of an oxygenated saline solution (NaC1 124 mM, NaHCO3 24 mM, NaH2POa 1.25 mM, KC1 6 mM, CaCI2 4 mM, MgSOa 2 mM, glucose 10 mM) under an atmosphere of moist 95 ~o 02-5 ~ COz. The bath K + concentration is approximately twice that of brain extracellular fluidS,n; this high level has been employed by previous workers using similar techniques 4,15,~9, and in our hands it favours the occurrence of synaptic activation comparable to that seen in the intact hippocampus. Some nerve fibres do, however, behave abnormally in 6 mM potassium in vitro and normally in 3 mM potassium s. In the present experiments the pO2 is higher than in vivo and the temperature lower: both these conditions favour the survival of relatively thick slices with the least damage to cells. In view of the various

Further studies of the potential-dependence of the sodium-induced membrane current in snail neurones.

1. The potential-dependence of the membrane current induced by intracellular injections of sodium ions was studied on giant neurones of the snail Helix pomatia. This current decreases with membrane hyperpolarization at room temperature and can be reversed at sufficiently negative holding potentials. The same injections at 7 degrees C, as well as injections of lithium or potassium ions do not induce membrane currents and do not increase membrane conductance. 2. An increase in the amount of injected sodium changes the potential-dependence of the induced membrane currents. Small injections (about 1 muC) induce a current that does not depend upon the membrane potential. Further increase in the injection size not only increases the induced current but also enhances its potential-dependence and often reveals the existence of a reversal potential. The latter reaches -60 to -65 mV with large sodium injections. 3. An increase in extracellular potassium concentration from 4 to 8 mM shifts the reversal potential 17 mV in the depolarizing direction, and a decrease from 4 to 2 mM shifts it 14 mV in the hyperpolarizing direction. Replacement of potassium by rubidium or elimination of sodium ions from the outside solution, does not affect the induced current or its potential-dependence. 4. The coefficient of electrogenicity (the ratio between the amount of charge transferred by the sodium-induced membrane current and the amount brought into the cell during the injection) increases with an increase in the injection size if the membrane potential is clamped near the resting potential level. This relation is reversed when the holding potential is -80 mV. The reversal takes place at holding potentials near -60 mV. 5. 10 mM TEA does not affect the induced current and its potential-dependence. 6. It is suggested that the potential-dependence of the sodium-induced membrane current is a result of a specific increase in the membrane potassium conductance that is coupled with high activity of the sodium pump.

A model of cell firing patterns during epileptic seizures.

A simplified model is presented of the dynamics of excitatory and inhibitory neurons in the cerebral cortex. A key feature of the model is that neurons may cease to fire when strongly depolarized (spike inactivation). Computer simulations for different parameters reveal five classes of solutons: a) steady states in which neither excitatory nor inhibitory cells are active, b) steady states in which one or both types of cells fire repetitively, c) states in which one type of cell fluctuates rapidly between bursts of action potentials and inactivity due to strong depolarization, d) rhythmic activity in which both types of cells fire in unison followed by a period of spike inactivation and e) states similar to d but in which the inhibitory cells never produce action potentials. Solutions b, c, d, and e qualitatively resemble the different firing patterns observed during experimental seizures. It is shown that changes in those parameters that are functions of potassium concentration can induce changes in the type of solution. It is therefore proposed that the increase in extracellular potassium concentration during seizures may be responsible for the progressive changes observed in firing patterns and particularly for the transition from tonic to clonic patterns. A method is also outlined for testing the predictions of the model.

On the mechanism of idioventricular pacemaker suppression by fast drive.

The role of vagal activity, potassium concentration, and temperature in overdrive suppression of ventricular pacemakers, was studied in anesthetized dogs with and without surgical atrioventricular block. The results were as follows. (1) Overdrive of an idioventricular pacemaker during vagal stimulation was followed by a second pause. (2) Hypothermia increased the duration of the vagal and overdrive pauses. (3) Coronary sinus plasma potassium concentration ([K] cs ) decreased with the onset of vagal stimulation and increased with overdrive during vagal stimulation. (4) The increase in [K] cs during ventricular overdrive was greater in hypothermia than it was in normothermia when the same absolute rate of overdrive was used and was unchanged when the same relative rate of overdrive was used. (5) Hypothermia increased overdrive suppression more than can be accounted for by the decrease in spontaneous rate, (6) By predriving the ventricles and then overdriving them, the increase in [K] cs was dissociated from the pause duration. It is concluded that during vagal stimulation ventricular arrest is due to the inhibition of idioventricular pacemakers by the sinus node by virtue of its faster rate and that changes in [K] cs are due to rate changes and not to acetylcholine release. Overdrive suppression can be dissociated from an increase in extracellular potassium concentration. Its prolongation in hypothermia provides evidence for a metabolism-dependent mechanism.

Work-induced increase of extracellular potassium concentration in muscle measured by ion-specific electrodes

Work-induced increase of extracellular potassium concentration in muscle measured by ion-specific electrodes

Water and electrolyte metabolism in skeletal muscle of exercising rats.

ArticleWater and electrolyte metabolism in skeletal muscle of exercising rats.P Kõrge, and A ViruP Kõrge, and A ViruPublished Online:01 Jul 1971https://doi.org/10.1152/jappl.1971.31.1.1MoreSectionsPDF (932 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEffect of extracellular osmolality on metabolism in contracting mammalian skeletal muscle in vitroApplied Physiology, Nutrition, and Metabolism, Vol. 34, No. 6Elemental composition of muscle at rest and potassium levels in muscle, plasma and sweat of horses exercising at 20°C and 35°C10 June 2010 | Equine Veterinary Journal, Vol. 28, No. S22Hematological and biochemical changes during a short triathlon competition in novice triathletesEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 61, No. 1-2Food deprivation decreases the exertion-induced acid hydrolase response in mouse skeletal muscleEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 57, No. 2Exhaustive physical exercise and acid hydrolase activity in mouse skeletal muscleHistochemistry, Vol. 57, No. 3Work-induced potassium changes in skeletal muscle and effluent venous blood assessed by liquid ion-exchanger microelectrodesPflügers Archiv European Journal of Physiology, Vol. 362, No. 1Analysis of the initial relaxation of mammalian skeletal muscles in ontogenyBulletin of Experimental Biology and Medicine, Vol. 76, No. 3Work-Induced potassium changes in muscle venous effluent blood measured by ion-specific electrodesPflügers Archiv European Journal of Physiology, Vol. 338, No. 2Effects of exercise and cold acclimation on the ventricular and skeletal muscles of white mice (Mus musculus)—I. Succinic dehydrogenase activityComparative Biochemistry and Physiology Part A: Physiology, Vol. 43, No. 4Work-induced increase of extracellular potassium concentration in muscle measured by ion-specific electrodesBrain Research, Vol. 40, No. 2 More from this issue > Volume 31Issue 1July 1971Pages 1-4 https://doi.org/10.1152/jappl.1971.31.1.1PubMed5556956History Published online 1 July 1971 Published in print 1 July 1971 Metrics

Transmembrane potential and contraction of human heart in relation to potassium and ouabain.

The effects of extracellular potassium chloride concentrations (0, 2, 4, 4.6, 5, and 8 mM.) on simultaneously recorded transmembrane action potentials and contractions of human papillary muscle were investigated. In a potassium-free solution the early changes observed were a shortening of the action potential duration (APD) at the 25% level of repolariza-tion, and no change or a slight increase in the APD at the 90% level of repolarization. A temporal relation between the shortening of the APD at the 25% and 50% levels of repolarization and an increase in the force of contraction was observed. A direct relation between the increase in extracellular potassium concentration and an increase in the APD as-sociated with a corresponding decrease in the force of contraction was observed. Ouabain (10-9 and 10-8 M.) produced a shortening of the APD and an increase in the contraction similar to KCl-free solution. Ouabain was ineffective in producing its effects on the muscles prein-cubated in KCl-free solution. Exposure of ouabain treated muscles to a KCl-free solution containing ouabain resulted in a small increase in the contraction and a small shortening of the APD of the muscles. The combined effects of ouabain and KCl-free solution were not greater than the effects of a KCl-free solution alone. It is suggested that the changes in APD and force of contraction might be associated with potassium or oua-bain-induced changes in the adenosinetriphosphatase activity of the heart muscle.

Mechanisms of intra-arterial Kplus-induced cardiovascular and respiratory responses.

ARTICLESMechanisms of intra-arterial Kplus-induced cardiovascular and respiratory responsesCT Liu, RA Huggins, and HE HoffCT Liu, RA Huggins, and HE HoffPublished Online:01 Oct 1969https://doi.org/10.1152/ajplegacy.1969.217.4.969MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByReflexes Controlling Circulatory, Ventilatory and Airway Responses to Exercise1 January 2011Divergence of ventilatory responses to isometric contraction in anesthetized catsRespiration Physiology, Vol. 104, No. 2-3Comparison of blood pressure and heart rate responses to isometric exercise and passive muscle stretch in humans1 March 1995 | European Journal of Applied Physiology and Occupational Physiology, Vol. 70, No. 3Blood pressure and heart rate during rest-exercise and exercise-rest transitionsEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 64, No. 2Cardiovascular reflexes during sustained handgrip exercise: role of muscle fibre composition, potassium and lactateEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 65, No. 4Reduction in extracellular muscle volume increases heart rate and blood pressure response to isometric exerciseEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 60, No. 3The influence of muscle interstitial volume on K+-induced heart rate drive in ratsEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 57, No. 1Response of chemosensitive nerve fibers of group III and IV to metabolic changes in rat musclesPfl�gers Archiv European Journal of Physiology, Vol. 410, No. 1-2Congestive cardiac failure: central role of the arterial blood pressure.Heart, Vol. 58, No. 3LiteraturRespiratory Control During Exercise1 January 2011Slowly Conducting Afferent Fibers from Deep Tissues: Neurobiological Properties and Central Nervous ActionsCirculation to Skeletal Muscle1 January 2011Cardiovascular Reflex Control by Afferent Fibers from Skeletal Muscle Receptors1 January 2011Cardiovascular Adjustments to Isometric Contractions: Static Effort1 January 2011Changes in heart rate and blood pressure upon injection of algesic agents into skeletal musclePfl�gers Archiv European Journal of Physiology, Vol. 393, No. 1ON REFLEX CONTROL OF EXERCISE HYPERPNEA FROM MUSCULAR RECEPTORSPERIPHERAL NEURAL CONTROL OF CARDIOVASCULAR AND RESPIRATORY RESPONSES TO ISOMETRIC EXERCISEReflex inputs to the cardiovascular and respiratory centers from dynamically working canine muscles. Some evidence for involvement of group III or IV nerve fibers.Circulation Research, Vol. 41, No. 3Effect of contraction on lymphatic, venous, and tissue electrolytes and metabolites in rabbit skeletal musclePfl�gers Archiv European Journal of Physiology, Vol. 368, No. 3Work-induced potassium changes in skeletal muscle and effluent venous blood assessed by liquid ion-exchanger microelectrodesPflügers Archiv European Journal of Physiology, Vol. 362, No. 1Work-Induced potassium changes in muscle venous effluent blood measured by ion-specific electrodesPflügers Archiv European Journal of Physiology, Vol. 338, No. 2Work-induced increase of extracellular potassium concentration in muscle measured by ion-specific electrodesBrain Research, Vol. 40, No. 2 More from this issue > Volume 217Issue 4October 1969Pages 969-973 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.217.4.969PubMed5824336History Published online 1 October 1969 Published in print 1 October 1969 Metrics

Effects of digitalis upon body electrolytes.

Studies of the electrolyte alterations in 54 dogs during 165 discrete digitalizations with acetyl strophantbidin to an endpoint of ventricular tachycardia are reported. In 94 per cent of digitalizatious, increase in arterial potassium concentration occurred. This was noted as early as five niinutes after drug administration. At the time of ventricular tachycardia, the increase was 0.67 mEq./L. When digitalization was carried to ventricular fibrillation, the increase was 3.1 mEq./L. In 75.5 per cent of the digitalizations, arterial sodium concentration decreased; average de crease was 2.6 mEq./L. At ventricular fibril lation, the decrease amounted to 11.0 mEq./L. Arterial calcium concentration and oxygen saturation were not altered. There was a modest decrease in CO 2 content and an increase in arterial pH and hcmatoerit. Peaking of the late portion of the T wave was common during acute digitalization and correlated with the increase in extracellular potassium concentration. The relationship of the electrolyte changes to the process of digitalization is discussed.