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PubMed2006

Alterations in uterine sodium pump abundance may contribute to the onset and progression of term and preterm labor in mice.

OBJECTIVE: Other investigators have shown that reductions in active sodium pump units increase uterine contractility. Therefore, our goal was to determine whether uterine sodium pump abundance is decreased in mouse models of term and preterm labor. STUDY DESIGN: Mice were studied during the final one-third of pregnancy. Other pregnant mice had preterm labor induced with lipopolysaccharide and were studied at timed intervals thereafter. Uterine sodium pump alpha3-isoform messenger RNA and protein were measured. Data were analyzed by analysis of variance. RESULTS: Uterine sodium pump alpha3-isoform messenger RNA fell significantly from day 14 to day 18 and remained low on the day of birth. Uterine sodium pump alpha3-isoform protein levels decreased significantly also. In lipopolysaccharide-induced preterm labor, uterine sodium pump alpha3-isoform protein, but not messenger RNA, decreased significantly. CONCLUSION: Sodium pump alpha3-isoform protein levels decreased in uterus before term labor and lipopolysaccharide-induced preterm labor. These findings are similar to those in humans, which suggests that this mouse model may be useful in the study of the sodium pump in human pregnancy. Reductions in sodium pump number can increase uterine contractile force and may contribute to labor.

Animals↗
PubMed1994

Sodium pump current measured in cardiac ventricular myocytes isolated from control and potassium depleted rabbits.

OBJECTIVE: The aim was to investigate cardiac muscle sodium pump function following chronic potassium depletion in rabbits. METHODS: Sodium pump current was measured using the whole cell voltage clamp technique in ventricular myocytes from control rabbits or rabbits with chronic dietary potassium depletion, under conditions designed to minimise all other electrogenic channels, pumps, and exchangers. The effects of changes in external [K+] and intracellular [Na+] were investigated. Experiments were performed on ventricular myocytes enzymatically isolated from adult rabbits, average weight 2.5 kg, which were fed either a control (n = 6), or a potassium deficient diet (n = 8) for 25 d. RESULTS: Potassium depletion significantly increased the sodium pump current density recorded with 10 mM extracellular [K+] and 50 mM [Na+] in the pipette (conditions which activate an estimated 98% of the maximally available pump current), from 1.53(SEM 0.05) pA.pF-1 (control, n = 4) to 1.740(0.06) pA.pF-1 (potassium depleted, n = 4; p < 0.05). The relationship between sodium pump current and extracellular [K+] (30 mM [Na+] in pipette) showed a significant leftward shift in myocytes from potassium depleted animals, such that the Km was reduced from 1.270(0.10) (control, n = 4) to 0.72(0.11) mM (potassium depleted, n = 4; p < 0.05). The effect of varying pipette [Na+] on sodium pump current was examined in cells superfused with 5 mM [K+]. The Km was again reduced from 19.44 mM (control) to 16.91 mM (potassium depleted). The Hill coefficients for activation of the pump by potassium and sodium were essentially unchanged, as was the shape of the current-voltage relationship. CONCLUSIONS: These results suggest that chronic potassium depletion results in an adaptation of the cardiac sodium pump such that pump activity can be maintained, or even enhanced, despite a fall in plasma [K+]. This adaptation is achieved by both alterations in ionic sensitivity to potassium and sodium, and an increase in maximum activity. The latter may reflect an increase in sodium pump site density. These changes are likely to account for the preservation of intracellular [K+] in cardiac muscle during chronic potassium deficiency.

Animals↗
PubMed1984

Acute stress stimulates the red cell sodium pump in rat.

The effect of restraint stress (RS) on the red cell sodium pump, hematocrit, plasma osmolality and plasma sodium and potassium concentrations was measured. Ten min of RS did not produce any change in the sodium pump activity. Longer lasting stress - 150 min - stimulated significantly the sodium pump activity in comparison to the control group (8.52 +/- 0.76 vs. 7.78 +/- 0.46 min-1 per 10(13) Ery; P less than 0.05; means +/- S.D.). Hematocrit rose during the stress (controls: 44.8 +/- 2.3; 10 min RS: 48.1 +/- 1.1; 150 RS: 47.0 +/- 1.9%; P less than 0.01 and P less than 0.05, respectively). The values for osmolality and plasma sodium concentration did not change. However, the plasma potassium concentration decreased significantly after 150 min of RS (4.63 +/- +/- 0.74 vs. 3.3 +/- 0.48 mmol 1(-1); P less than 0.001). Thus, acute stress stimulates the sodium pump activity in erythrocytes of the rat and norepinephrine seems most likely to trigger this activation.

Animals↗
PubMed1990

Relationship between the maximum velocity and sodium affinity of the erythrocyte sodium pump and its rate constant in blood.

1. Young and mature erythrocytes from 15 normal subjects were used to compare the sodium pump rate constant measured in whole blood with the more definitive sodium affinity constant and maximum velocity of the sodium pump measured in artificial media using sodium-loaded cells. 2. Similar values were obtained from both erythrocyte fractions for the sodium affinity constant and maximum velocity and also by using two different plots. The median error in the estimate of individual sodium affinity constants and maximum velocities from regression analysis was about 20% and the precision was not improved by combining the data points for the two erythrocyte fractions. 3. The rate constant in whole blood was closely related to the sodium affinity constant and maximum velocity of the sodium pump (r = 0.75), suggesting that it was a reasonable overall assessment of available sodium pump activity. 4. Differences in the rate constant between subjects were due to differences in both the maximum velocity and sodium affinity constant of the sodium pump so that the rate constant could not be used as a guide to the underlying sodium pump physiology.

Adult↗
PubMed2003

Changes in the isoforms of the sodium pump in the placenta and myometrium of women in labor.

OBJECTIVE: We determined whether changes in sodium pump isoform abundance accompanied active human labor. STUDY DESIGN: Specimens of placenta, amniochorion, and myometrium were collected from women in active spontaneous labor and from those not in labor. The abundance of the three sodium pump alpha-isoforms was determined by Western blot analysis. RESULTS: Levels of the alpha1 and alpha2 isoforms were comparable in the three tissues for women in labor and not in labor. However, alpha3 isoform abundance in placenta and myometrium (but not amniochorion) was significantly decreased in women in active labor compared with women not in labor (sodium pump alpha3 in placenta: no labor 91.2 +/- 27.6 vs labor 46.9 +/- 3.6 density units, P =.002. Sodium pump alpha3 in myometrium: no labor 52.3 +/- 7.7 vs labor 19.8 +/- 1.6 density units, P =.0002). CONCLUSION: Because reductions in sodium pump number can result in hormone release from secretory tissues and in contraction of muscle, this suggests that the sodium pump may play a significant role in the initiation or maintenance of human labor.

Adult↗
PubMed1992

Sodium pump failure in hypoxia and reoxygenation.

Sodium pump measurements have not been previously documented in the intact heart close to the onset of irreversible injury in hypoxia and reoxygenation. In the present experiments, Rb+ uptake was measured in the presence and absence of ouabain in Langendorff-perfused rat hearts. In the presence of ouabain, Rb+ uptake was increased after 10 min hypoxia (P < 0.05 vs. controls), but not after 30 min hypoxia, suggesting transient activation of a passive pathway such as the ATP-sensitive K+ channels. Passive Rb+ uptake was normal during post-hypoxic reoxygenation. Active Rb+ uptake was reduced after 30 min hypoxia, increased on reoxygenation after 10 min hypoxia, and failed to recover on reoxygenation after 30 min hypoxia (P < 0.001, P < 0.05 and P < 0.001, respectively, vs. controls). Sodium pump failure may lead to calcium overload through sodium-calcium exchange, and may be a decisive influence in post-hypoxic reoxygenation injury.

Animals↗
PubMed1998

Bovine adrenals contain, in addition to ouabain, a second inhibitor of the sodium pump.

In the search for endogenous cardiac glycosides, two different inhibitors of the sodium pump have been isolated from bovine adrenals. Inhibitor A with a molecular mass of 600 Da and a UV maximum at 250 nm was purified from 16 kg of bovine adrenals. The pure substance (<1 ng) inhibited the sodium pump of human red blood cells with an affinity similar to that of ouabain, yet it cross-reacted with antibodies against the bufadienolide proscillaridin A but not against the cardenolide ouabain. Inhibitor A was slightly more hydrophilic than ouabain on RP-C18 high pressure liquid chromatography. Hence, it showed properties similar to the proscillaridin A immunoreactivity (Sich, B., Kirch, U., Tepel, M., Zideck, W., and Schoner, W. (1996) Hypertension 27, 1073-1078) that increased in humans with systolic blood pressure and pulse pressure. Inhibitor B of the sodium pump with a molecular mass of 584 Da was purified 10(6)-fold from 20 kg of bovine adrenals. It cross-reacted with antibodies against ouabain but not with antibodies against proscillaridin A and inhibited the sodium pump of human and rat red blood cells with the same affinity as ouabain. All other properties, such as the retention time in a C18-reversed phase chromatography, molecular mass determination by electrospray mass spectrometry and fragmentation pattern, and UV and 1H NMR spectroscopic data, were identical to ouabain. Hence, sodium pump inhibitor B from bovine adrenals is the cardenolide ouabain.

Adrenal Glands↗
PubMed1978

Studies on the crystalline lens. XXVI. Kinetic study showing saturation of the sodium pump.

Active transport of sodium out of rabbit lenses was shown to be carrier mediated by observing the dependence of efflux of 22Na on intracellular concentration of nonlabeled sodium which previously was elevated by incubating lenses at 0 degree C. Velocity of sodium efflux increased asymptotically with increasing concentrations of intracellular sodium, demonstrating saturation of the carrier. The maximum velocity of the sodium pump based on Michaelis-Menten kinetics was found to be 4.6 mumol/hr/lens, and the half-saturation of the carrier, which appeared to involve a single site, occurred at 36 mM.

Animals↗
PubMed1988

Thyroxin specifically stimulates anuran larvae epidermal sodium pump during metamorphosis.

1. Sodium pump, measured as K+-dependent, ouabain sensitive pNPPase, but not the non-specific, ouabain insensitive pNPPase, was stimulated by thyroxin in epidermis of tadpoles of Rana perezi. 2. Epidermal K+-pNPPase of thyroxin treated tadpoles was only stimulated in those stages already showing activity and reached levels similar to adult frogs in tadpoles at metamorphic climax.

Animals↗
PubMed2006

Effects of sodium pump activity on spontaneous firing in neurons of the rat suprachiasmatic nucleus.

Cell-attached and whole cell recording techniques were used to study the effects of electrogenic sodium pump on the excitability of rat suprachiasmatic nucleus (SCN) neurons. Blocking the sodium pump with the cardiac steroid strophanthidin or zero K+ increased the spontaneous firing of SCN neurons to different degrees with different recording modes, whereas turning the sodium pump into a nonselective cation channel with the marine toxin palytoxin invariably increased the spontaneous firing to the point of total blockade. Current-clamp recordings indicated that strophanthidin increased the rate of membrane depolarization and reduced the peak afterhyperpolarization potential (AHP), whereas zero K+ also increased the rate of depolarization, but enhanced the peak AHP. The dual effect of zero K+ was reflected by the biphasic time course of voltage responses to zero K+: an inhibitory phase with enhanced peak AHP and slower firing, followed by a delayed excitatory phase with faster rate of membrane depolarization and faster firing. In the presence of strophanthidin to block the sodium pump, zero K+ consistently decreased firing by enhancing the peak AHP. Repetitive applications of K+ -free solution gradually turned the biphasic inhibitory-followed-by-excitatory voltage response into a monophasic inhibitory response in cells recorded with the whole cell (but not the cell-attached) mode, suggesting rundown of sodium pump activity. Taken together, the results suggest that spontaneous firing of SCN neurons is regulated by sodium pump activity as well as the AHP, and that sodium pump activity is modulated by intracellular soluble substances subject to rundown under the whole cell conditions.

Acrylamides↗
PubMed2002

Endogenous ligand of alpha(1) sodium pump, marinobufagenin, is a novel mediator of sodium chloride--dependent hypertension.

BACKGROUND: Digitalis-like sodium pump ligands (SPLs) effect natriuresis via inhibition of renal tubular Na(+),K(+)-ATPase but may induce vasoconstriction. The present study investigated the potential roles of 2 putative endogenous SPLs, an ouabain-like compound (OLC) and an alpha(1) Na(+),K(+)-ATPase inhibitor, marinobufagenin (MBG), in regulating natriuresis and blood pressure (BP) responses to sustained and acute NaCl loading in Dahl salt-sensitive rats (DS). METHODS AND RESULTS: During 4 weeks of an 8% NaCl diet, DS exhibited a progressive increase in MBG renal excretion (66 +/-13 pmol/24 hours at week 4 versus 11 +/- 1 pmol/24 hours at baseline, n=48), which paralleled an increase in systolic BP (174 +/- 10 mm Hg at week 4 versus 110 +/- 2 mm Hg at baseline). By contrast, OLC excretion peaked at week 1 and returned to baseline levels. Administration of an anti-MBG, but not anti-ouabain antibody, to DS after 3 weeks of a high NaCl diet lowered BP (139 +/- 7 versus 175 +/- 5 mm Hg, P<0.001, n=5). Acute NaCl loading (2 hours) of DS (n=5) increased MBG and OLC excretion and natriuresis. Pretreatment of acutely NaCl-loaded DS with an anti-MBG antibody (n=5) reduced the excretion of sodium and MBG but not that of OLC. An anti-ouabain antibody (n=5) reduced sodium excretion and both OLC and MBG. CONCLUSIONS: An initial transient stimulation of OLC induced by NaCl loading of DS precedes an MBG response. A sustained increase in MBG production in DS contributes to the chronic BP elevation induced by a sustained high NaCl intake.

Adrenal Glands↗
PubMed1986

Non-esterified fatty acids may regulate human leucocyte sodium pump activity.

Human leucocyte sodium pump activity was studied in normal fasting subjects by measuring the ouabain-sensitive 22Na+ efflux rate constants. This 22Na+ efflux rate constant was inversely related to the fasting plasma non-esterified fatty acid level (rs = -0.73, P less than 0.0001). An oral glucose load (40 g/m2 surface area) led to an increase in the leucocyte ouabain-sensitive 22Na+ efflux rate constant after 2 h (1.97 +/- 0.25 to 2.44 +/- 0.19 h-1, P less than 0.0001, n = 11). There was a concomitant fall in the plasma non-esterified fatty acid level. Incubation of leucocytes in vitro with 100 mumol/l linoleic acid inhibited the leucocyte ouabain-sensitive 22Na+ efflux rate constant (1.52 +/- 0.27 vs 0.84 +/- 0.24 h-1, P less than 0.001, n = 8). The leucocyte Na+,K+-dependent adenosine triphosphatase (Na+,K+-ATPase) activity was inhibited in vitro by long chain non-esterified fatty acids, especially when unsaturated. Non-esterified fatty acids may account for some of the Na+,K+-ATPase inhibitory activity of plasma.

Biological Transport, Active↗
PubMed1975

Different approaches to the mechanism of the sodium pump.

The way in which the sodium pump uses energy from the hydrolysis of ATP to perform osmotic and electrical work is not yet understood. We attempt to bring together the results of a number of different approaches to this problem. One approach has been to correlate biochemical changes and ionic fluxes, both when the pump operates normally and when it operates in various abnormal 'modes' in particular unphysiological conditions. A second approach has been to expose fragments of cell membrane to (gamma-32P)ATP and to study the properties of components of the membrane that become labelled. It is now clear that 32P can be transferred to the beta-carboxy group of an aspartyl residue in a pump polypeptide, but there is controversy about the interrelations of different forms of this polypeptide and its role, if any, in the normal functioning of the pump. A third approach has been to attempt to purify the pump and to determine the properties of the pure enzyme. It seems that the pump contains a polypeptide (molecular weight about 100,000), which bears the phosphorylation site, and a smaller glycopeptide, but there is disagreement about the molecular ratios. The results of these and other approaches cannot yet be fitted into a satisfactory model for the sodium pump, but we shall consider some of the problems involved in this task.

Adenosine Diphosphate↗
PubMed1996

Role of skeletal muscle sodium pumps in the adaptation to potassium deprivation.

Skeletal muscle is specialized to lose K+ to the extracellular fluid during potassium deprivation which buffers the fall in plasma K+ concentration. While it remains to be determined whether K+ efflux from muscle is altered during K+ deprivation, active K+ uptake driven by sodium pumps is significantly depressed. The activity of sodium pumps in skeletal muscle does not increase during K+ depletion despite elevated intracellular Na+, a strong stimulus to increase activity in other cells. There is a decrease in the total pool size of sodium pump alpha beta heterodimers during potassium deprivation. The alpha 2 (not the alpha 1) sodium pump isoform is specifically decreased and beta 1 and/or beta 2 decreases in a muscle-fibre-dependent manner. The specific loss of K+ from skeletal muscle is probably a consequence of the fact that the alpha 2 isoform predominates in this tissue. In tissues such as heart, where alpha 2-type pumps are only a minor fraction of the sodium pumps, the activity of the ubiquitous alpha 1 isoform maintains intracellular Na+ and K+ at control levels, despite the fact that alpha 2 levels decrease by 50%. Analysis of the time course of change in alpha 2 mRNA vs. protein during K+ deprivation indicates that there is both a decrease in alpha 2 synthesis and an increase in alpha 2 degradation. The apparent time-lag during potassium deprivation between the early decreases in both surface alpha 2-type sodium pump number (assessed by 3H-ouabain binding) and intracellular K+, and the later decrease in total pool size of alpha 2, suggests the hypothesis that there may be an early internalization of alpha 2 sodium pumps to endosomal pools, followed by a degradation of these internalized pumps, contributing to the decrease in total alpha 2 pool size. The signals mediating this specific response to hypokalemia, and those mediating the restoration of muscle K+ stores remain to be determined.

Animals↗
PubMed1990

Sodium pump numbers and cation transport of lymphocytes in pregnancy-induced hypertension.

Pregnancy-induced hypertension may be linked with sodium pump inhibition and an increase in vascular myocytic tone and, hence, flow impedance. All of the findings of studies on circulating plasma and blood cells are not, however, consistent with this hypothesis. We therefore assessed sodium pump numbers and cation transport in lymphocytes from 23 women with untreated pregnancy-induced hypertension, 28 normotensive pregnant women and 28 healthy non-pregnant women. We measured the maximum 3H-ouabain binding capacity to determine the sodium pump activity and the apparent dissociation constant (the reciprocal of which estimates binding affinity) by Scatchard analysis, ouabain-sensitive (pump-mediated) 86rubidium influx and ouabain-resistant (pump-independent) influx in lymphocytes in vitro. Pregnant women, whether normotensive or hypertensive, had significantly more sodium pump activity and a higher pump-mediated and pump-independent 86rubidium influx than non-pregnant women. Sodium pump activity and the pump-mediated and pump-independent 86rubidium influx all reached normal, non-pregnant levels in normotensive pregnant women 6 weeks after delivery, but remained high in women with pregnancy-induced hypertension. The normotensive and hypertensive pregnant women and non-pregnant women all had similar ouabain binding affinity. The results of our study do not support the circulating sodium pump inhibitor hypothesis in pregnancy-induced hypertension.

Adult↗
PubMed1996

Palytoxin-induced Na+ influx into yeast cells expressing the mammalian sodium pump is due to the formation of a channel within the enzyme.

Palytoxin forms ionic channels in animal cell membranes but does not have similar effects on bacteria or yeast cells. These channels appear to be associated with the sodium pump. Using a heterologous expression system for the mammalian sodium pump in the yeast Saccharomyces cerevisiae, we recently demonstrated palytoxin-induced K+ efflux from yeast cells. Using the same system, we now show that the palytoxin-induced Na+ influx measured by others in animal cells is also directly associated with the sodium pump. Under the influence of palytoxin, yeast cells that express the mammalian sodium pump exchange extracellular Na+ ions for intracellular K+ ions with a stoichiometry of approximately 1:1. Both fluxes can be inhibited by ouabain. K+ efflux can also be observed when extracellular Na+ is replaced by Li+, Cs+, or NH4+. These data suggest that all palytoxin-induced ion fluxes measured so far in various cell systems are directly associated with the sodium pump. Palytoxin-induced Na+ influx or K+ efflux does not occur with yeast cells that express a truncated form of the sodium pump that is missing 44 of the carboxyl-terminal amino acids of the alpha 1 subunit. Scatchard analysis reveals only a slightly lower affinity of the truncated form for [3H]ouabain compared with the affinity of the native enzyme. Yeast cells expressing the truncated enzyme can bind [3H]ouabain, which can be displaced by palytoxin. Therefore, the inability of the truncated form to conduct ions under the influence of palytoxin is not due to the removal of the palytoxin binding site but rather to the removal of a part of the enzyme that participates in a direct or indirect way in the formation of the palytoxin-induced channel. Based on these findings, we conclude that palytoxin opens a channel within and not merely in the vicinity of the sodium pump. This might be the same channel that under normal conditions actively transports Na+ and K+ ions.

Acrylamides↗
PubMed1987

Sodium pump activity in young and adult salt hypertensive Dahl rats.

The possible role of endogenous sodium pump inhibitors was studied in salt-sensitive rats of Dahl strain which were influenced by high salt intake either in youth (from prepuberty) or only in adulthood. The aim of our study was to search for the relations between the age-dependent blood pressure response to high salt intake and the changes in volume or distribution of body fluids, red cell ion transport or Na+,K+-ATPase activity in various tissues of salt-sensitive (S/JR) and salt-resistant (R/JR) rats. Salt hypertension was especially pronounced in those S/JR rats which were maintained on a high-salt diet from prepuberty. This was accompanied by the moderate expansion of body fluids in young but not in adult hypertensive animals. Na+,K+-ATPase activity was suppressed in both kidney and heart of young S/JR rats with salt hypertension while this was not true in adult hypertensive animals. On the other hand, no inhibition of sodium pump was observed in brain microsomes and erythrocytes of severely hypertensive young S/JR rats. Moreover, no increased levels of endogenous sodium pump inhibitors were detected in plasma of salt hypertensive S/JR rats. Thus our study indicated the age-dependent suppression of sodium pump activity in some tissues of salt hypertensive Dahl rats but we failed to confirm increased levels of circulating sodium pump inhibitors in young salt hypertensive rats.

Aging↗
PubMed1994

Modulation defect of sodium pump evidenced in diabetic patients by a microcalorimetric study.

Sodium pump activity of intact erythrocytes in their own plasma was measured by microcalorimetry in 41 healthy subjects and 35 insulin-dependent diabetic patients. Results show that modulation of the sodium pump is altered in diabetic patients. Addition of insulin increases functioning of the Na(+)-K+ pump in controls but has no effect in diabetic patients. These subjects show a slower response of the Na(+)-K+ pump to the inhibitory effect of ouabain. Cross-incubation experiments suggest that these findings may be explained by the existence of a plasmatic factor that impairs the modulation of the sodium pump in diabetic patients.

Adult↗