Net Loss Of Potassium Research Articles

Agricultural Intensification and Soil Fertility in Atlantic Spain, 1750–1890

AbstractThis article describes the intensification process of agriculture and its environmental limits regarding soil fertility in the rural community of Fonsagrada, in the inner region of Galicia in northwestern Spain. It addresses changes in land use, crops, and agricultural productivity between 1750 and 1890, framed within the theory of social metabolism and based on the method of nutrient balances. That technique measures nitrogen, phosphorus, and potassium flows across the landscape within a given agro-ecosystem to assess its biophysical functioning and to detect environmental constraints related to management. The intensification of cropland resulted in net losses of potassium in outlying rough grazing land and hay meadows that served as the sources of cropland nutrients. Agricultural intensification was possible due to the close stabling of livestock, which allowed for more manure availability. Doing so, however, deprived pastureland of nutrient recover through manure deposition, which created a metabolic rift in the agro-ecosystem.

Ratio of sodium to potassium in the Mercury exosphere

The ratio of sodium to potassium in the exosphere of Mercury is highly variable and averages about 100, considerably larger than for the Moon. We considered the possibility that this high value results from potassium loss rates that are larger than sodium loss rates. The principal loss processes are the sweeping of hot atoms off the planet by solar radiation acceleration and the capture of metal photoions by the solar wind. We found that radiation acceleration losses are not sufficiently different for sodium and potassium to explain the high ratio. Capture of sodium and potassium photoions by the solar wind is thought to be the major loss process. However, there is a competing process for the ions, which is collision with the surface, followed by neutralization. These atoms can return to the exosphere. The net steady state density of sodium and potassium in the exosphere depends on the relative efficiencies of solar wind capture and surface recycling. We propose that the photoion loss and recycling rates are sufficiently different for sodium and potassium to account for the high ratio. The higher mass of the potassium atom relative to sodium results in a smaller scale height and a larger gyroradius for potassium relative to sodium, which may result in more rapid net loss of potassium.

Characterization of cell volume loss in CEM-C7A cells during dexamethasone-induced apoptosis.

A reduction in cell volume is a fundamental feature of apoptosis. We have characterized changes in cell volume, together with nuclear changes, occurring in dexamethasone-induced apoptosis in CEM-C7A lymphoblastoid cells. Cell volume was measured by electronic cell sizing and flow cytometry, and two distinct phases of volume loss were observed. The first phase began 12 h after addition of dexamethasone (5 microM) and progressed until 36 h when chromatin condensation was detected in intact cells. Removal of dexamethasone before 36 h (the precommitment period) resulted in reversal of the volume decrease and prevented the appearance of nuclear changes. Cell shrinkage in the first 24 h of dexamethasone exposure was associated with a net loss of potassium but no change in cellular buoyant density. There were no significant differences in the rates of volume recovery after either hypertonic or hypotonic stimuli. These observations favor a mechanism of cell shrinkage involving loss of the entire cytoplasmic contents, possibly following proteolysis, rather than loss of only osmolytes and water. The second phase of volume loss was coincident with chromatin condensation and was associated with cellular fragmentation and a reduction in cellular density. We conclude that volume loss in this model of apoptosis is mediated by multiple mechanisms that are both dependent and independent of cellular fragmentation.

Potassium loss during myocardial ischaemia and hypoxia: does lactate efflux play a role?

In heart, the available evidence suggests that transmembrane lactate flux is mediated predominantly by an H(+)-lactate transporter with properties similar, but not identical, to the H(+)-monocarboxylate transporter present in many other tissues. Passive (electro-)diffusion of HL and L- comprise only minor components of total transmembrane lactate flux over the range of lactate concentrations relevant to normal physiological and pathophysiological states. The cardiac H(+)-lactate transporter is non-electrogenic, and transport is partially inhibited by potassium, possibly by competition for the H+ binding site on the carrier. However, K+ is cotransported with lactate very inefficiently, if at all, compared to H+. From these observations, a direct mechanism coupling potassium efflux to lactate efflux, by either an electrogenic or a non-electrogenic mechanism, is unlikely to account for the majority of net potassium loss during myocardial ischaemia or hypoxia, unless the properties of transmembrane lactate flux are markedly altered by the ischaemic and hypoxic environment. Nevertheless, it is intriguing that alterations in pHi, pHo, and transmembrane pH gradients in ischaemic cardiac muscle and fatigued skeletal muscle have effects on net potassium loss that qualitatively parallel the predicted effects on L- efflux. In view of the lack of evidence for a direct link between potassium and lactate efflux in the heart, it is likely that this apparent relationship is either coincidental or indirect, mediated through a series of intermediate transport processes. The nature of these interactions remain to be defined. Further studies are still needed to solve the puzzle of what causes net cellular potassium loss during myocardial ischaemia and hypoxia.

Input and Output of Nutrients in a Diked Flooded Savanna

Nutrient mass balances in forest ecosystems have been well studied, but there is a lack of information concerning input and output of nutrients in savanna ecosystems (llanos). The south-western Venezuelan llanos are seasonally flooded; therefore an extensive network of dikes has been built to alleviate the floods and retain water throughout the dry period. Net losses of calcium and magnesium in Mantecal's diked savanna were in general lower than the values found in other ecosystems. Net losses of potassium in diked flooded savannas surpassed the value existing for forested ecosystems indicating that, although the diking did not induce a dramatic change in nutrient budgets, it nevertheless affected the magnitude of output for this critical element (...)

Acceptability of Intermittent Handgrip Contractions Based on Physiological Response

Our aim was to study physiological response and acceptability of intermittent muscle contractions. Seven male subjects performed eight isometric handgrip exercises with altered contraction-relaxation periods but identical tension-time products. Local blood flow (BF), heart rate, blood pressure, electromyography, maximal voluntary handgrip contraction (MVC), and venous concentration of potassium and lactate of both forearms were followed during and up to 24 hours after the exercises. Wrist force response to electrical stimulation of a forearm muscle was used to investigate low-frequency fatigue (LFF). Ratings of perceived exertion were recorded during exercise. LFF was associated with a decreased functional capacity, which may be explained by a net potassium loss. Recovery BF was linearly related to mean contraction intensity of the experiments. Physiological criteria for acceptability of isometric exercise are suggested, based on the absence of fatigue during exercise and the return to baseline values within four hours of the recovery period. Based on these physiological criteria, intermittent handgrip contractions at (or higher than) a mean contraction intensity of 17% MVC and continuous handgrip contractions at (or higher than) 10% MVC were considered unacceptable.

Exercise‐induced hyperkalaemia can be reduced in human subjects by moderate training without change in skeletal muscle Na, K‐ATPase concentration

In 15 conscripts, venous plasma potassium was followed during exercise on a training bicycle before and after 10 weeks of moderate physical training and a putative relationship with skeletal muscle Na,K-ATPase was evaluated. Peak plasma potassium concentration obtained at exhaustion was 6.1 +/- 0.2 and 5.6 +/- 0.2 mmol l-1 (mean +/- SEM, n = 14, P less than 0.05) before and after training, respectively. Throughout the exercise period and within the first minutes of rest plasma potassium concentration was 0.2-0.5 mmol l-1 higher before than after training. Neither peak values nor peak rises in plasma potassium concentration before nor after training were correlated to the 3H-ouabain binding site (Na,K-ATPase) concentration in vastus lateralis muscle. The results indicate that net loss of potassium from the skeletal muscle pool during exercise is reduced after training, that the heart during exercise may be exposed to a smaller rise in plasma potassium concentration after training than before, and that moderate improvement of capacity to clear extracellular potassium during exercise may be due to increased activity of existing Na,K-pumps in resting skeletal muscle fibres. This may reduce muscle fatigue, increase physical performance and explain the paradoxical observation that, despite an increased catecholamine response, there is a reduced risk of cardiac events after training.

Alanine stimulation of passive potassium efflux in hepatocytes is independent of Na(+)-K+ pump activity

We have studied the effects of alanine on electrolyte content and ion transport in rat hepatocytes in primary culture. Application of 10 mM alanine is followed by 1) an increase in the rate of sodium entry; 2) an increase in intracellular sodium content; 3) an increase in ouabain-inhibitable rubidium uptake, a measure of Na(+)-K+ pump rate; 4) an increase in unidirectional potassium efflux, whether or not the Na(+)-K+ pump was inhibited; and 5) an increase in the initial rate of potassium loss after Na(+)-K+ pump inhibition. This increase occurred even when alanine was presented in Ringer made hypertonic by the addition of sucrose. Application of hypotonic solution led to a significant net loss of potassium, but no net loss of potassium was observed after alanine application. Thus alanine stimulates the Na(+)-K+ pump by increasing intracellular sodium secondary to an increase in the rate of sodium entry. Passive potassium efflux is stimulated by a mechanism that is independent of the stimulation of the Na(+)-K+ pump. The stimulated potassium efflux does not appear to be a response to cell swelling.

Effects of sampling conditions on selected blood variables of rainbow trout, Salmo gairdneri Richardson

The effects of two methods of specimen immobilization (MS 222 anaesthesia and stunning), two types of anticoagulant (EDTA and heparin), two storage temperature ranges (0–2°C and 22–25°C) and four sample storage periods (0, 1, 3, and 24 h) on the haemoglobin, haematocrit, plasma and packed cell sodium, potassium and chloride ion concentrations and packed cell ATP levels of rainbow trout were examined. Stored samples exhibited increases in cell volume, net transfer of sodium and chloride from plasma into cells, net loss of potassium to plasma and rapid depletion of ATP. Room temperature conditions and prolonged storage exacerbated these changes. Use of EDTA, particularly in combination with MS 222, frequently led to haemolysis. Least change in most variables was observed in samples drawn from stunned specimens, treated with heparin and refrigerated before use or preparation for deep cold storage.

Extracellular K + and H + shifts in early ischemia: Mechanisms and relation to changes in impulse propagation

Heart and skeletal muscle cells rapidly lose potassium ions after withdrawal of oxygen. In myocardial ischemia, cellular release of potassium and interruption of extracellular washout produce a rapid and marked increase of extracellular K+ concentration. Harris et al. were the first to observe the coincidence of the K+ shift and the frequent occurrence of ventricular arrhythmias. They ascribed a major role to K+ in the genesis of the electrophysiological changes in early ischemia. The purpose of this article is to outline briefly in the first part the relationship between potassium accumulation and the electrical changes in ischemia with emphasis on reviewing the role of K+ in the slowing of impulse propagation and production of conduction block. In the second part, the possible mechanisms leading to potassium imbalance will be discussed and experimental data will be presented which suggest that an important component of net potassium loss is related to the development of acidosis.

Recovery from decamethonium in rat muscle and denervated guinea-pig diaphragm.

1. In denervated guinea-pig diaphragm the depolarization produced by decamethonium (100 microM) was followed by an initial phase of recovery, and then by a slow restoration of membrane potential in the presence of the drug, with hyperpolarization. Membrane potentials were measured by repeated insertions. The slow phase of spontaneous recovery was not found in the absence of potassium or in the presence of ouabain (100 microM). 2. With 1 microM-decamethonium the net loss of potassium from denervated muscle was 17% by wet weight in 20 min as compared with controls, which represents a loss of over 30 mM in internal concentration. Similar results were obtained with 100 microM-decamethonium. Spontaneous recovery of potassium occurred in the succeeding 2 h in the presence of 1 microM and 100 microM-decamethonium. With 5 nM-decamethonium muscles exposed for 20 min had a potassium content which was not reduced as compared with controls. 3. In rat diaphragm decamethonium (100 microM) also produced depolarization and slow spontaneous recovery which was not seen in the absence of potassium or the presence of ouabain. With 3 mM-decamethonium spontaneous recovery of potential was complete in 5 min. 4. Change from 5 mM-potassium to potassium-free solution produced consistent hyperpolarization in denervated guinea-pig diaphragm. In rat diaphragm at 38 degrees C the results were variable, with some fibres showing hyperpolarization while others showed depolarization.

Effect of ouabain in therapeutic concentrations on K+ exchange and contraction of human and rabbit myocardium.

1. Experiments were undertakn on strips of human atrial and ventricular muscle, on right ventricular rabbit papillary muscles and on the rabbit interventricular septum. 2. In all preparations an increase of developed tension after 30 min exposure to ouabain was apparent only at or above a concentration of 10(-7) mol/l (73 micrograms/l). 3. In the rabbit septum there was a net loss of potassium on exposure to ouabain if the concentration was greater than 10(-7) mol/l. There was no net loss, or gain, of potassium at lower concentrations. Loss of potassium, indicating inhibition of the sodium pump, could not be dissociated from the positive inotropic effect of ouabain. 4. The greater sensitivity to ouabain of human myocardium in vivo (10(-8) mol/l) than in vitro (10(-7) mol/l) may be due to cellular changes occurring in isolated preparations.

Effects of catecholamines, ATP and ionophore A23187 on potassium and calcium movements in isolated hepatocytes

IN addition to their well known effects on hepatic gluconeogenesis and glycogenolysis, adrenaline and noradrenaline cause a transient net loss of potassium from the liver of many species1. Studies with guinea pig and rabbit liver slices have shown this to be a consequence of a predominantly α -adrenoceptor-mediated increase in the potassium permeability (PK) of the hepatocyte membrane2–4. It has recently become possible to isolate hepatocytes in high yield and with cation levels and metabolic capabilities superior to those of slices, and approaching that of the intact tissue5. We have now confirmed that the effects of catecholamines on potassium movement can be shown with such cells, and we have obtained evidence to support the suggestion that the potassium loss which follows α-adrenoceptor activation in guinea pig liver cells is a consequence of an increase in potassium permeability triggered by a rise in intracellular calcium. The mechanism can be blocked by quinine, as in human erythrocytes19 and barnacle photoreceptors20.

Potassium activity in photoreceptors, glial cells and extracellular space in the drone retina: changes during photostimulation.

1. A double-barrelled potassium-sensitive micro-electrode was developed that was fine enough to record intracellular electrical potentials and potassium activities (aK) in the drone retina. 2. aK was measured in the photoreceptor cells, in the pigment (glial) cells, and in the extracellular space, in the superfused, cut, retina. The effect of photostimulation was studied: 20 msec light flashes, intense enough to evoke receptor potentials of maximum amplitude were presented, 1/sec, in a train lasting about 2 min. 3. In photoreceptors with membrane potentials greater than or equal to 50 mV aK in the dark was 79 mM, S.D. = 27 mM, n = 11. During photostimulation aK fell by 21.5 +/- 9.5 mM with a half-time of 30 +/- 22 sec. (A tentative conversion from activities to free concentrations can be made by taking the activity coefficient as 0.70 its value in the Ringer solution). 4. In pigment cells with membrane potentials greater than or equal to 50 mV, aK in the dark was 52 mM, S.D. = 13 mM, n = 11. During photostimulation aK increased by 14 +/- 5 mM. 5. In the extracellular space aK increased during photostimulation with a mean half-time of less than 1.3 sec to a maximum (mean value 14 mM, S.D. = 8.4 mM, n = 22), and then fell to a plateau. 6. It is estimated from the anatomy that the photoreceptors occupy approximately 38% of the total volume of the retina, the pigment cells 57%, and extracellular space 5%. Hence, it seems possible that during photostimulation nearly all the net loss of potassium from the photoreceptors is temporarily stored in the pigment cells. 7. Recordings were made in the extracellular space of the intact animal by passing the electrode through a hole in the cornea. The mean aK in the dark was 7.7 mM, S.E. = 0.4 mM, n = 22. In the superfused retina, aK in the dark was 6.3 mM, S.E. = 0.7 mM, n = 22, even though aK in the Ringer solution was 2.2 mM. Increasing the aK of the Ringer solution to 7.0 mM had no apparent effect on aK in the extracellular space at depths greater than 20 micron. 8. In the intact animal the amplitude and time course of the change in extracellular aK evoked by the standard pattern of photostimulation were within the range observed in the superfused preparation.

Nutrient Cycling in a Eucalyptus obliqua (L'hérit.) Forest. II. A Study in a Small Catchment

The geochemical balance of cations (input in rainwater-output in stream-water) in a mature E. obliqua forest is shown to be dependent primarily on the amount of 'stream-water' leaving the catchment at the weir. During the 3 complete years of the study, the annual balance of calcium was positive, the annual balance of magnesium was negative, and there was either a net gain or net loss of sodium and potassium depending on the amount of stream-flow. The order of mobility is sodium > potassium > magnesium > calcium, in accord with physicochemical properties. More calcium than sodium is returned annually from plant to soil by litter fall and leaching (biogeochemical cycling), yet the rate of loss of calcium in stream-water is less than one-twentieth that of sodium. The ecosystem is described as 'tight' in respect to calcium (the annual geochemical balance is con- sistently small relative to the amount cycled biogeochemically) and 'loose' in respect to sodium (the annual geochemical balance is highly variable with a range equal to the annual biogeochemical cycle). The annual turnover in litter fall and leaching of calcium plus magnesium plus potassium represents 9% of the amount of these elements in the above-ground biomass. The geochemical balance, however, is only +0. 13 % of the amount in the biomass, and thus the biogeochemical cycling of these elements in the mature forest appears to be at equilibrium. Introduction

Potassium exchange and mechanical performance in anoxic mammalian myocardium.

Mechanical performance and 42K exchange were studied during anoxia in isoalted, arterially perfused, interventricular rabbit septa at 42 beats/min and 28 degree C. The septa were perfused at 1.8 ml/min per g with a modified Tyrode solution having dextrose as the metabolic substrate. Developed tension declined to 16% of preanoxic control values during 60 min of anoxia, and returned to 65% of control during a 60-70 min recovery. Anoxia induced net potassium losses of 31+/-2, 53+/-2, and 90+/-14 mmol K+/kg dry tissue (means+/-SE) during 20, 40, and 60 min of anoxic stresses, determined by tissue probe analysis after asymptotic labeling. Potassium losses attributed to increased efflux of the ion from the cells during 20, 40, and 60 min of anoxia were determined from effluent analyses to be 32+/-4, 60+/-6, and 98+/-11 mmol K+/kg dry wt. Potassium loss began within seconds of the onset of anoxia and reoxygenation immedaitely reversed the potassium loss. These data indicate that 1) function of the membrane Na-K pump is maintained through 60 min of anoxia with the entire net potassium loss attributable to increased efflux from the cells, 2) anoxia decreases the rate of exchange of potassium after recovery, and 3) the cell membrane appears to be the rate-limiting site of potassium efflux during anoxia.

Temperature effect on sodium and chloride movements in larval Ambystoma gracile

Abstract o 1. Unidirectional sodium and chloride fluxes and net potassium loss were measured on animals acclimated to 5, 15 and 25°C. These measurements were also made on animals after acutely increasing or decreasing their temperature 10 or 20°C. 2. Na and Cl unidirectional fluxes are not affected the same by a 10 or 20°C increase in temperature. 3. Results are discussed in the light of postulated sodium-cation and chloride-anion exchanges.

Chemical characteristics of traumatic spinal cord edema in cats. Effects of steroids on potassium depletion.

✓ Edema of the spinal cord, secondary to an impact injury produced in cats, was measured chemically. One day after injury a decrease in percentage dry weight and potassium concentration and an increase in sodium concentration were seen in the injured cord. By the second day these changes had spread to adjacent tissue. Edema was maximal between the third and sixth day and had begun to recede by the ninth day. A net loss of potassium, not directly related to the edematous changes, was observed throughout the analyzed cord starting on the third day and persisting on the ninth day after injury, when edema was regressing. Dexamethasone, started 48 hours before or 5 or 24 hours after injury had only minimal effect on edema but prevented loss of potassium from the injured cord. Six days after injury this effect was statistically significant in all three groups of dexamethasone-treated animals. All treated animals showed significantly better functional recovery than the untreated cats. On the sixth post-injury day the functional state of all animals was highly correlated with the potassium content of the spinal cord. Thus, the beneficial effect of dexamethasone may be related to the postulated role of steroid treatment in the maintenance of structural integrity of cellular elements in traumatized tissues. This could result in a better functional state of the injured cord, as well as in the maintenance of the normal content of potassium, the principal intracellular ion.

Effects of warm ischemia on the potassium and sodium contents and on the sodium-, potassium-ATPase activity in dog kidney slices.

The potassium and sodium contents in dog kidneys were studied after various warm ischemia times. A considerable net loss of potassium as well as a gain of sodium were demonstrated during the first hou

The effects of indomethacin on calcium, sodium, potassium and magnesium fluxes in various tissues of the guinea-pig.

1. Isolated tissues of the guinea-pig were bathed with Krebs solution at 37 degrees C and subjected to 100 ms pulses of electrical stimulation for 30 min at a frequency of 0.1 or 1.0 Hz. The tissues were then dried, ashed, and the ash analysed for calcium, sodium, potassium and magnesium.2. Gastric smooth muscle, cardiac and skeletal muscles and brain all showed a gain of sodium and calcium and a loss of potassium in response to electrical stimulation, but there was no significant change in the magnesium content of any of these tissues.3. Indomethacin (0.5 mM) reduced the calcium content of unstimulated gastric smooth muscle and reduced the gain of calcium and sodium in response to electrical stimulation, but slightly increased the net loss of potassium in response to electrical stimulation.4. Gastric smooth muscle which had gained calcium as a result of electrical stimulation, gradually lost it again when stimulation ceased. Indomethacin (0.5 mM) hastened the net loss of calcium from previously stimulated muscle.5. Indomethacin (0.5 mM) failed to alter the calcium, sodium, potassium and magnesium contents of unstimulated cardiac muscle, skeletal muscle and brain. In these tissues indomethacin (0.5 mM) also failed to prevent the changes in the content of these minerals which occurred in response to electrical stimulation.