Movement Of Potassium Research Articles

A further characterization of the selective K movements observed in human red blood cells following acetylphenylhydrazine exposure.

Following brief exposure to acetylphenylhydrazine, the potassium permeability of the human erythrocyte membrane is selectively augmented. While a similar increase in potassium permeability results from the intracellular accumulation of calcium (the Gardos phenomenon), we have found a number of features that allow these two pathways to be distinguished from one another. The acetylphenylhydrazine pathway does not require calcium for its activation, and can be seen even in the presence of a molar excess of the calcium chelator EGTA. The transmembrane potassium movement via this channel has a specific requirement for the anion chloride, and it can be inhibited by furosemide. The potassium that moves through the Gardos pathway, on the other hand, can be accompanied by any permeant anion, and is inhibitable by quinidine or cetiedil. Thus, acetylphenylhydrazine exposure seems to promote K + Cl cotransport, whereas the Gardos pathway represents a potassium conductive channel. While full demonstration of both these pathways requires harsh in vitro manipulation, the large electrochemical potassium gradient favoring the movement of this cation out from the erythrocyte suggests that even a partial activation of either pathway could cause intracellular dehydration and thus contribute importantly to the pathophysiology of in vivo red cell destruction.

Movement of potassium in an Ustochrept soil profile in a long-term fertilizer experiment

SummaryDownward movement of potassium (K) was studied in the soil profiles of a longterm fertilizer experiment. The distribution of different forms of K and the percentage K saturation of the CEC of soil, at various depths of the differentially treated plots, indicated that applied K moved down to 75 cm depth in the high-K plots after nine cycles of a maize-wheat-cow peas crop rotation. However, movement of K was not noticed in plots not given K fertilizers. Plant uptake of K far exceeded the amounts of applied K. Application of K fertilizer reduced the release of K from the non-exchangeable reserves. Forms of K and the percentage K saturation of the CEC of soils were significantly correlated.

Inhibition of clathrin-coated vesicle acidification by duramycin.

Clathrin-coated vesicles contain a proton translocating ATPase which operates in parallel with a chloride transporter (Xie, X.-S., Stone, D.K., and Racker, E. (1983) J. Biol. Chem. 258, 14834-14838). The polypeptide antibiotic, duramycin, has a dual inhibitory effect on clathrin-coated vesicle acidification. Low amounts of duramycin (5 micrograms/100 micrograms of protein) inhibit by 50% the proton translocation facilitated by chloride translocation. Under these conditions duramycin inhibits also 36Cl uptake when driven by either the electrogenic proton pump or by inward directed K+ movement in the presence of valinomycin. Higher amounts of duramycin (20 micrograms/100 micrograms of protein) are needed to inhibit by 50% the proton pump itself, as evidenced by reduced proton translocation facilitated by an outward potassium movement in the presence of valinomycin. In addition, the amount of duramycin needed to inhibit the proton pump corresponded well with the amount needed to inhibit the ouabain-insensitive, N-ethylmaleimide-sensitive ATPase activity of clathrin-coated vesicles.

Cyclic AMP stimulates ouabain-insensitive ion movement in shark rectal gland

When the active sodium-potassium pump (Na−K-ATPase) of shark rectal glands is blocked by ouabain, the concentration of intracellular ions changes in the direction of equilibrium with extracellular fluid. These changes were examined when isolated perfused glands were in the basal state and also when they were stimulated to secrete with cAMP and theophylline, to see whether stimulation affected the passive movement of sodium, potassium and chloride across cell membranes. In basal glands 10−4M ouabain induced an increase of 30 meq/l in intracellular [Na+] and a decrease in intracellular [K+] of about 50 meq/l after 30 min, while intracellular [Cl−] was unchanged. In stimulated glands, these movements were exaggerated. The increase in intracellular [Na+] averaged 112 meq/l, and the decrease in intracellular [K+], 96 meq/l (P<0.01), while mean intracellular [Cl−] rose by 80 meq/l. Furosemide, 10−4M, partially reversed the accelerated changes in intracellular electrolytes seen after ouabain was added to stimulated glands. These results are consistent with an action of cAMP upon a ouabaininsensitive cotransport of sodium, potassium and chloride in the rectal gland, analogous to that described in avian erythrocytes.

Corticosteroid alteration of active electrolyte transport in rat distal colon.

To determine the effect of corticosteroids on active transport processes, unidirectional fluxes of 22Na, 36Cl, and 42K were measured under short-circuit conditions across isolated stripped distal colonic mucosa of the rat in control, secondary hyperaldosterone, and dexamethasone-treated animals. In controls net sodium and chloride fluxes (JNanet and JClnet) and short-circuit current (Isc) were 6.6 +/- 2.2, 7.6 +/- 1.6, and 1.3 +/- 0.2 mu eq X h-1 X cm-2, respectively. Although aldosterone increased Isc to 7.3 +/- 0.5 mu eq X h-1 X cm-2, JNanet (6.9 +/- 0.7 mu eq X h-1 X cm-2) was not altered and JClnet was reduced to 0 compared with controls. Dexamethasone also stimulated Isc but did not inhibit JClnet. In Cl-free Ringer both aldosterone and dexamethasone produced significant and equal increases in JNanet and Isc. Theophylline abolished JNanet in control animals but not in the aldosterone group. Aldosterone reversed net potassium absorption (0.58 +/- 0.11 mu eq X h-1 X cm-2) to net potassium secretion (-0.94 +/- 0.08 mu eq X h-1 X cm-2). Dexamethasone reduced net potassium movement to 0 (-0.04 +/- 0.12 mu eq X h-1 X cm-2). These studies demonstrate that 1) corticosteroids stimulate electrogenic sodium absorption and 2) aldosterone, but not dexamethasone, inhibits neutral NaCl absorption and stimulates active potassium secretion. The effects of mineralocorticoids and glucocorticoids on electrolyte transport are not identical and may be mediated by separate and distinct mechanisms.

Response of cochlear potentials to presumed alterations of ionic conductance: endolymphatic perfusion of barium, valinomycin and nystatin.

Two models ('single-pump' and 'two-pump') of transepithelial potassium movement by the marginal cells of the stria vascularis have been proposed in the literature. Their validity was considered by exposing the endolymphatic (luminal) surface to agents (barium, valinomycin and nystatin) which are known to alter specific cellular membrane conductances in other tissues. This was accomplished by the use either of injections or of a relatively satisfactory technique for perfusion of scala media, which is described. Injection of barium caused the endocochlear potential (EP) to increase in normal animals and had no effect on the EP of deaf, Waltzing guinea pigs. Perfusion of the ionophores caused a decline in the EP in both normal and Waltzing guinea pigs. Only the 'two-pump' model (Na/K-ATPase-mediated cation pump on the basolateral membrane and rheogenic K transporter at the luminal membrane) is consistent with the results. The cellular heterogeneity of the cochlear duct, however, introduces a measure of uncertainty into this interpretation.

Effect of Baking and Frying on Nutritive Value of Potatoes: Minerals

ABSTRACTThe effect of conventional baking and frying on the mineral content of Katahdin, Chipbelle and Rosa varieties of potatoes was investigated. The cortex and pith tissues of the tubers were used. Conventional baking reduced the cortical content of potassium, phosphorus, and iron by 10–13%, 4–21%, and 19–31% respectively. In all three varieties, movement of potassium, phosphorus, and iron toward the interior tissues was demonstiated during conventional baking although varieties varied widely in their mineral content. Conventional baking increased the pith content of potassium (14–23%), phosphorus (2–9%), and iron (2–8%). Frying decreased significantly all the minerals in both the cortical and pith areas with the major loss occurring in the cortical area (10–45%).

Sodium and potassium transport in ferret red cells.

Potassium movements into ferret red cells were measured with the tracer 86Rb. Equilibration of 86Rb between medium and cells could be resolved into two components. 70-90% occurred rapidly with a rate constant of between 3.5-5.5 h-1. The remaining 10-30% occurred slowly. The slow movement was equivalent to a potassium influx of about 1.2-2.76 mmol l-1 cell h-1. Potassium influx was inhibited by 80-90% by 0.1 mM-bumetanide (a high-ceiling, loop diuretic). This suggests that the sodium-potassium co-transport system has a high capacity for carrying potassium (estimated at about 17-35 mmol l-1 cell h-1). After bumetanide (0.1 mM) remaining potassium movements (approximately 0.5 mmol l-1 cell h-1) are at a similar level to that found in red cells from other animals. The sodium pump makes a very small contribution to potassium flux into ferret red cells. Much of this pump activity may be attributed to reticulocytes present in cell samples. Sodium movements across the red cell membrane were measured with 22Na. Sodium equilibrated more slowly than potassium. 60-70% of the sodium influx was inhibited by 0.1 mM-bumetanide, indicating that most sodium influx in ferret red cells is also through the co-transport system. The co-transport system can transport up to 49 mmol sodium l-1 cell h-1 and is half maximally activated by 0.38 mM-potassium in the external medium. In the presence of bumetanide, sodium influx (about 18 mmol l-1 cell h-1) is similar to that of other carnivore red cells. This is about five times greater than that of red cells from non-carnivores. The possibility that there are two populations of ferret red cells with different potassium transport characteristics is discussed.

Modification of potassium movement through the retina of the drone (Apis mellifera male) by glial uptake.

Intracellular recordings were made in photoreceptors and glial cells (outer pigment cells) of the superfused cut head of the honey-bee drone (Apis mellifera male). When the [K+] in the superfusate was abruptly increased from 3.2 mM to 17.9 mM both photoreceptors and glial cells depolarized. The time course of the depolarization of the photoreceptors was slower with increasing depth from the surface. Half time of depolarization was plotted against depth: this graph was compatible with the arrival of K+ being exclusively by diffusion through the extracellular clefts. However, as we then showed, this interpretation is inadequate. The time course of depolarization of the glial cells was almost the same at all depths. This indicates that they are electrically coupled. Consequently, current-mediated K+ flux (spatial buffering) through glial cells will contribute to the transport of K+ through the tissue: K+ ions enter the glial syncytium in the region of high external potassium concentration, [K+]0, and an equivalent quantity of K+ ions leave in regions of low [K+]0. Intracellular K+ activity (aiK) was measured with double-barrelled K+-sensitive micro-electrodes in slices of retina superfused on both faces. When [K+] in the superfusate was increased from 7.5 mM to 17.9 mM an increase in aiK was observed in glial cells at all depths in the slice (initial rate 1.7 mM min-1, S.E. of the mean = 0.2 mM min-1), but there was little increase in the photoreceptors (0.3 +/- 0.2 mM min-1). The increase in aiK in glial cells near the centre of the slice could not have been caused by spatial buffering; it presumably resulted from net uptake. We conclude that when [K+] is increased at the surface of this tissue, the build up of K+ in the extracellular clefts depends on extracellular diffusion, spatial buffering and net uptake. The latter two processes, which have opposing effects, involve about 10 times as much K+ as the first. This is in rough agreement with less direct experiments on mammalian brain (Gardner-Medwin, 1977, 1983b).

Hemolytic action of potassium salts on dog red blood cells

Recent demonstrations of chloride-associated passive potassium movements in red blood cells of humans, ducks, sheep, and toadfish prompted a reinvestigation of potassium permeability in dog red blood cells. Early observations of Davson (J. Physiol. London 101:265-283, 1942) had shown that replacement of chloride by nitrate and thiocyanate caused a greatly increased rate of potassium flux across the dog red cell membrane. This finding seemed at variance with results in other species in which chloride replacement caused a fall in potassium flux. The present data indicate that passive potassium movements in swollen dog red blood cells are chloride dependent and furosemide sensitive, as shown for the cells of other species. Davson's findings were demonstrated to be due to the inclusion of small quantities of calcium in the medium under circumstances that favored calcium entry into the cells, thus opening the calcium-activated potassium channel described by Gardos (Curr. Top. Membr. Transp. 10:217-277, 1978 and Nature London 279:248-250, 1979). Potassium movements through the latter channel were stimulated when chloride was replaced by more permeant anions, such as nitrate and thiocyanate, which also increased the rate of net potassium movements in valinomycin-treated cells.

Differential calcium dependence of contractile responses and 86Rb efflux from the rabbit aorta induced by vasoactive stimuli.

86Rb was used to monitor potassium movements in strips of rabbit aorta simultaneously with measurements of tension. Histamine, noradrenaline, the prostaglandin endoperoxide analogue U46619, angiotensin II, and 144 mM K+ each induced an increase in 86Rb efflux concomitantly with contraction. For the first four agonists there was a rank-order correlation between the contractile response and 86Rb efflux, but 144 mM K+ induced a massive increase in 86Rb efflux although it was the weakest contractile stimulus. Contraction and increase in 86Rb efflux-induced K+ were both reduced by verapamil, which blocks voltage-sensitive calcium channels, implying that both effects of K+ were mediated mainly by a depolarisation-induced influx of calcium. Noradrenaline increased both tension and 86Rb efflux through an action on alpha-adrenoceptors, but its effect on efflux, unlike its effect on tension, was apparently totally dependent on the presence of extracellular calcium. Experiments performed in the presence of lanthanum, which blocks calcium influx, showed that the intracellular store of calcium released by noradrenaline apparently played no role in inducing 86Rb efflux, although it could trigger contraction. Lanthanum also blocked contraction induced by K+ but had less effect on the increase in 86Rb efflux induced by K+. Thus, agonist-induced vascular contraction and 86Rb efflux can be dissociated, but under normal conditions all the contractile stimuli tested induced 86Rb efflux.

Basolateral potassium channel in turtle colon. Evidence for single-file ion flow.

Treatment of the apical surface of the isolated, ouabain-inhibited turtle colon with the polyene antibiotic amphotericin B permitted the properties of a barium-sensitive potassium conductance in the basolateral membrane to be discerned from the measurements of transepithelial fluxes and electrical currents. Simultaneous measurements of potassium currents and 42K fluxes showed that the movement of potassium was not in accord with simple diffusion. Two other cations, thallium and rubidium, were also permeable and, in addition, exhibited strong interactions with the potassium tracer fluxes. The results indicate that permeant cations exhibit positive coupling, which is consistent with a single-file mechanism of ion translocation through a membrane channel.

Cyclic Adenosine Monophosphate Stimulates Active Potassium Secretion in the Rat Colon

To determine whether cyclic adenosine monophosphate influences active potassium transport in the rat colon, we studied the effect of dibutyryl cyclic adenosine monophosphate and theophylline on unidirectional transmural 42K fluxes across proximal colonic mucosa under short-circuited conditions. Active potassium secretion (-0.19 +/- 0.02 microEq/h X cm2) was present in animals maintained on a normal potassium diet. Both 0.5 mM dibutyryl cyclic adenosine monophosphate and 5 mM theophylline significantly increased net potassium secretion by 0.49 +/- 0.04 and 0.33 +/- 0.03 microEq/h X cm2, p less than 0.001, respectively; the stimulation of net potassium secretion was secondary to an increase in serosal-to-mucosal potassium transport without change in mucosal-to-serosal potassium movement. A similar increase in active potassium secretion (from -0.15 +/- 0.03 to -0.32 +/- 0.03 microEq/h X cm2, p less than 0.005) was produced by bethanechol, a cholinergic muscarinic agonist that alters sodium and chloride transport by a noncyclic adenosine monophosphate, calcium-dependent process. In animals maintained on a high potassium diet, active potassium secretion was significantly increased to -0.79 +/- 0.17 microEq/h X cm2 (p less than 0.001). In these potassium-loaded animals, theophylline produced a greater increase in active potassium secretion (0.91 +/- 0.10 vs. 0.33 +/- 0.03 microEq/h X cm2, p less than 0.001) than in animals fed a normal potassium diet. These studies demonstrate that cyclic adenosine monophosphate and noncyclic adenosine monophosphate mediated secretogogues stimulate active potassium secretion. We speculate that the mechanism by which cyclic adenosine monophosphate increases active potassium secretion is related to an increase in luminal potassium conductance.

A comparative study of electrolyte absorption from the caecum and colon of Oryctolagus cuniculus—II. Sodium and potassium

1. 1. The movements of sodium and potassium across the wall of large intestine in anaesthetized rabbits have been studied. 2. 2. At colonic level the relationship between the sodium absorption rate and its intraluminal concentration depends on the initial conditions. 3. 3. In caecum or colon, sodium absorption occurs from intraluminal levels lower than the plasma ones. 4. 4. At colonic level, potassium is secreted for concentrations similar to the plasma ones.

Role of the medullary collecting duct in potassium conservation.

A capacity for both net potassium absorption and net potassium secretion has been demonstrated in the inner medullary collecting duct. The quantitative importance, however, of the inner medullary collecting duct in the regulation of urinary potassium in potassium deficiency, however has not been established. To assess the contribution of this segment to potassium conservation, microcatherization studies were performed in male Sprague-Dawley rats maintained either on a control diet or on a potassium free diet for 72 h. In control animals approximately 15% of the filtered load of potassium was excreted. Analysis of tubule fluid along the inner medullary collecting duct failed to demonstrate evidence of net potassium movement. Administration of a potassium free diet resulted in a marked reduction in potassium excretion to 0.3% of the filtered load. In contrast to control the inner medullary collecting duct of experimental animals absorbed nearly 90% of the amount of potassium entering this segment, since fractional delivery to the terminal portion of the nephron was about 2%. These data indicate that the inner medullary collecting duct makes a significant contribution to maximal renal conservation of potassium, since previous studies have shown that only 5 to 10% of filtered potassium is present in the late distal tubule of surface nephrons in animals on a low potassium intake.

Glia and the control of potassium movement in cortex

Active neurons release K + during synaptic potentials as well as action potentials. Since neurons are surrounded by narrow extracellular clefts, K + accumulation in these clefts may be expected, and indeed has been detected in vertebrate brain and squid axon. What mechanisms are available for removing extracellular K + so that it does not interfere with neural function? Previously, extracellular diffusion and active cellular re-uptake were regarded as the main mechanisms 8. Recent work by Tony Gardner-Medwin suggests that passive redistribution by a glial ‘spatial buffer’ makes a significant contribution.

Acetylcholine and potassium-42 movements in right atrial muscle of the guinea pig

The effect of acetylcholine (ACh) on potassium (K-42) movements has been studied in right atrial tissue of the guinea pig. When quiescent fibers were stimulated at 108 beats/min, potassium uptake was increased to a small but significant extent. Administration of acetylcholine (2.7 × 10 −6 M) induced an increase in potassium uptake that was greater in fibers that were quiescent than in the same fibers when stimulated. The ACh induced increase in potassium uptake was abolished by atropine (5.2 × 10 −7 M) and enhanced in the presence of nicotine (10 −5 M). In addition, ACh induced an increase in potassium efflux that was greater in fibers that were quiescent than in the same fibers when stimulated. Atropine blocked the effect of ACh on potassium efflux. It is concluded that activity of atrial tissue increases potassium uptake and modifies the action of ACh on potassium uptake and efflux. Muscarinic receptors mediate the ACh induced increase in potassium movements. Nicotinic receptors may mediate an ACh induced decrease in potassium uptake in atrial muscle.

The effect of gamma-aminobutyric acid on the potassium movements of rat cortical synaptosomes.

K+ fluxes of rat cortical synaptosomes were monitored by a K+ sensitive ion-selective membrane electrode. The uptake phases of K+curves from control and experimental measurements were compared and statistically evaluated. GABA significantly reduced K+ uptake but it was able to reverse the decrease of K+ uptake caused by protoveratrine. In the absence of Ca2+ the K+ uptake was diminished; GABA had no effect on this inhibition. The effect of GABA on K+ take was partially reduced by bicuculline and abolished by diamino-butyric acid. The K+ content of synaptosomes decreased, while the NA+ content increased in the presence of GABA. The results are discussed in association with presynaptic depolarisation and with modulatory effects of GABA on the release of other transmitters.

Demonstration of net potassium absorption in mammalian colon.

The present in vivo studies were performed in the rat to determine whether the colon was capable of net potassium absorption, as well as secretion, and to further elucidate the process responsible for net potassium movement. Both the proximal and distal lumina of the colon of control, potassium-deficient, and potassium-loaded animals were perfused with solutions containing either 140 or 20 mmol/l sodium. Net potassium secretion was present in both proximal and distal colon of control animals during perfusion with the 140 mmol/l sodium solution. The rate of net potassium secretion was reduced in the potassium-deficient animals. During perfusion with the 20 mmol/l sodium solution, the rate of potassium secretion was also reduced (compared with control perfusion solution) in both the control and potassium-deficient animals. As a result, there was net potassium absorption (0.94 +/- 0.14 mueq.1-1.g dry wt-1) and zero net potassium movement in the distal and proximal segments, respectively, of the potassium-deficient animals perfused with the low-sodium solution. Additional studies were performed to determine whether net potassium secretion was saturable and showed that, during progressive increases in the plasma potassium level, net secretion was constant at plasma potassium levels above 11-13 meq/l. These data, therefore, demonstrate that the mammalian colon regulates intestinal transport of potassium by both absorptive and secretory mechanisms and that a carrier-mediated process probably regulates both transport processes.

Effect of cetiedil, an in vitro antisickling agent, on erythrocyte membrane cation permeability.

Cetiedil has been reported to relieve painful crises in sickle cell anemia and to have antisickling properties in vitro. The drug alters neither oxygen affinity nor the solubility of deoxyhemoglobin S. Because the viscosity of the erythrocyte interior and the kinetics of gelation are dependent on the concentration of hemoglobin, we postulated that cetiedil might inhibit sickling by modifying erythrocyte sodium or potassium movements in a manner that would increase cell water content and thus dilute the cell hemoglobin. The drug has two such effects: it inhibits the specific increase in potassium permeability that follows a rise in cytoplasmic calcium concentration and it causes a rise in passive sodium movements. These effects are further evidence that cell ion and water movements may be important in the process of sickling and suggest a mechanism for the results reported with cetiedil.