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PubMed1992

Pregnancy induced hypertension and sodium pump function in erythrocytes.

OBJECTIVE: To determine if erythrocyte sodium pump function is altered with the onset of pregnancy induced hypertension. DESIGN: A prospective descriptive study. SUBJECTS: Thirty-two primigravid women with pregnancy-induced hypertension (17 had proteinuria) and 32 gestation-matched normotensive primigravid pregnant women were studied and measurements repeated 20 weeks after delivery. INTERVENTION: Erythrocyte sodium, ouabain-sensitive sodium flux and the sodium pump rate constant were measured in whole blood and the maximum velocity and sodium affinity of the sodium pump were measured in vitro. RESULTS: Blood pressure remained higher after delivery in the women who had been hypertensive during pregnancy. In normal pregnancy erythrocyte sodium was decreased, and ouabain-sensitive sodium flux, the sodium pump rate constant and maximum velocity (Vmax) were increased compared with 20 weeks after delivery. In pregnancy-induced hypertension erythrocyte sodium and sodium pump changes were the same as in normal pregnancy. The possibility of a positive association between changes in erythrocyte sodium and in blood pressure was excluded. The rate constant of the sodium pump in blood was related to its Vmax measured in vitro but the relation had greater variance in the hypertensives with 7 of the 32 women having rate constants greater than expected from their Vmax. CONCLUSION: There was no evidence of sodium pump inhibition or a rise in intracellular sodium associated with increased blood pressure in pregnancy. There may have been stimulation of the sodium pump by a plasma factor in some hypertensive women.

Adult↗
PubMed1992

Membrane incorporation of non-esterified fatty acids and effects on the sodium pump of human erythrocytes.

1. Sodium pump function has been assessed by measurement of ouabain-sensitive 86Rb uptake in human erythrocytes after incorporation of palmitic, stearic, oleic and linoleic acids into the erythrocyte membrane. 14C-labelled fatty acids were used to measure membrane uptake of these substances. 2. For palmitic, oleic and linoleic acids, up to 1000 nmol of the fatty acid/ml of packed cells can be incorporated without causing significant haemolysis. For stearic acid, 270 nmol/ml of packed cells was incorporated in similar conditions. More than 88% of the fatty acid incorporated could be extracted with a 50 mumol/l fatty-acid-free albumin solution and was, therefore, in a non-esterified form in the erythrocyte membrane. The concentrations of palmitic, stearic, oleic and linoleic acids incorporated in these experiments represent a five- to ten-fold increase above the normal concentrations of these fatty acids in the membrane. 3. Up to 1000 nmol of palmitic, oleic and linoleic acids/ml of packed cells and up to 270 nmol of stearic acid/ml of packed cells could be incorporated without a significant change in mean ouabain-sensitive 86Rb uptake with respect to control cells. Mean percentage changes in ouabain-sensitive 86Rb uptake for all these experiments were: palmitic acid, 3.7% (SD 11.4, n = 15); stearic acid, 4.0% (SD 5.7, n = 7); oleic acid, -4.8% (SD 19, n = 17); linoleic acid, 2.2% (SD 15.6, n = 19). 4. The demonstration of near-normal sodium pump activity in the presence of greatly elevated membrane levels of these fatty acids makes it extremely unlikely that they act as modulators of sodium pump function in vivo.

Cells, Cultured↗
PubMed1990

A serial study of erythrocyte sodium content and sodium pump kinetics in pregnancy.

1. Normotensive primigravid pregnant women were studied longitudinally during pregnancy and 20 weeks after delivery. 2. Erythrocyte sodium content, ouabain-sensitive sodium flux and sodium pump rate constant were measured in whole blood, and the maximum velocity and sodium affinity of the sodium pump were measured in vitro. 3. Erythrocyte sodium content decreased and the sodium pump rate constant increased up to 26 weeks gestation. The increase in rate constant was due to an increase in the affinity of the sodium pump for sodium up to 20 weeks gestation. After 20 weeks gestation there was an increase in maximum velocity and a decrease in sodium affinity of the sodium pump but no further change in the sodium pump rate constant. 4. At 14 weeks gestation the sodium pump rate constant was correlated with both the maximum velocity and sodium affinity constant. After this time the relationship was much more variable and there was no correlation with the sodium affinity constant. The comparison of measurements of the sodium pump in whole blood and in vitro gave no evidence of sodium pump inhibition. 5. The erythrocyte sodium pump changed throughout gestation with different components to the change, but, overall, available sodium pump activity in blood increased and sodium content decreased.

Biological Transport, Active↗
PubMed1996

Molecular activity of sodium pumps in endotherms and ectotherms.

Previous research has shown ectotherms to have markedly lower sodium pump metabolism than endotherms. Direct measurement of enzymatic activity of the sodium pump (Na(+)-K(+)-adenosinetriphosphatase) confirmed this difference. To determine the source of this difference, sodium pump density was measured with the use of [3H]ouabain binding. Ectotherms and endotherms were found to share similar sodium pump numbers. Approximate densities (in pmol/g) were 250 for skeletal muscle, 500 for liver, 900 for heart, and 8,000 for kidney and brain. Therefore, differences in sodium pump activity between endotherms and ectotherms were due to differences in turnover rates or molecular activities of sodium pumps. Molecular activities of sodium pumps (in ATP/min) of tissues from endotherms were between 6,000 and 12,000 and, for ectotherms, between 1,500 and 2,500. Exceptions were found that included the heart of Bufo marinus. In a single invertebrate species studied, Charax destructor, the sodium pumps of the heart had a low molecular activity characteristic of ectothermic tissues. These results suggest that during the evolution of endothermy there was a general increase in the molecular activity of the sodium pump.

Amphibians↗
PubMed1995

Endothelial stimulation of sodium pump in cultured vascular smooth muscle.

We studied vascular sodium pump activity and its regulation by vasoactive agents and endothelium in cultured aortic vascular smooth muscle cells from normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Baseline sodium pump activity (ouabain-inhibitable 86Rb+ uptake) was similar in cells from both rat strains. Angiotensin II and endothelin-1 increased ouabain-inhibitable 86Rb+ uptake more in SHR than WKY cells, whereas no effects were obtained with sodium nitroprusside, 8-bromo-cGMP, or iloprost. We examined the influence of endothelium on vascular sodium pump activity either by coculturing smooth muscle and endothelial cells or by using conditioned medium. Both coculture for 24 hours with endothelial cells and treatment with conditioned medium increased smooth muscle cell sodium pump activity, this effect being higher in SHR cells. These results suggest that the endothelium may modulate sodium pump activity in the underlying smooth muscle by releasing a diffusible compound, which is more active on SHR smooth muscle. The conditioned medium obtained in the presence of inhibitors of angiotensin-converting enzyme, endothelin-1-converting enzyme, cyclooxygenase, lipoxygenase, and nitric oxide synthase had no effect on the ability of conditioned medium to increase sodium pump activity, suggesting that angiotensin II, endothelin-1, eicosanoids, and nitric oxide are not involved in this stimulatory effect. The nature of the possible endothelial factor involved is still unknown, but it possesses a molecular weight between 25 and 50 kD, is heat stable, and is sensitive to trypsin treatment. We propose it could be a growth factor.

Animals↗
PubMed1984

Phasic vascular sodium pump changes in deoxycorticosterone-hypertensive rats.

We determined the sodium pump activity, measured as ouabain-sensitive 86Rb+ uptake, in the tail arteries of rats treated with deoxycorticosterone and sodium chloride for 6, 9, 14, 28, and 50 days. Systolic blood pressures, plasma sodium, potassium, and creatinine concentrations were measured, and the body weights were recorded. Vascular sodium pump activity was suppressed (by 27%) at the 6th day of deoxycorticosterone and sodium chloride treatment, a prehypertensive state. By the 9th day, blood pressure of deoxycorticosterone-treated and sodium chloride rats had increased, but sodium pump activity was not different from that of control animals. However, increases in sodium pump activity were noted after 14 and 28 days of deoxycorticosterone and sodium chloride treatment (18 and 21%, respectively). By 28 days, a fully developed hypertension was noted. At 50 days, rats displayed lower vascular sodium pump activity (by 23%) than the controls. These rats, although hypertensive, had significantly lower systolic blood pressures than the rats treated for 28 days. They had high plasma creatinine levels, low potassium and sodium concentrations, and low body weights compared to the controls, suggesting the presence of a malignant state. Our data indicate that there are time-related changes in the vascular sodium pump activity with this type of hypertension.

Animals↗
PubMed1994

Osmotic regulation of sodium pump in rat brain synaptosomes: the role of cytoplasmic sodium.

The effect of hypoosmolality of incubation medium on the rat of ouabain-sensitive 86Rb+ transport in rat brain synaptosomes was studied. A decreased osmolality from 310 to 250 mOsm increased the rate of 86Rb+ uptake from 3.72 to 6.23 nmol/mg of protein min. To evaluate the involvement of cytoplasmic sodium in sodium pump stimulation inhibitors of ion channels and transport pathways able to increase [Na+]in were used. Tetrodotoxin (1 microM), amiloride (0.5 mM) and verapamil (0.1 mM) had no influence on the osmotic response of the sodium pump. The decrease of sodium concentration in incubation medium to 15 mM, leading to a practical loss of its transmembrane gradient, did not abolish stimulation of pump. No increase in 22Na+ influx or intrasynaptosomal sodium content was registered at hypotonic conditions. It is suggested that osmotic regulation of Na+,K(+)-ATPase is not connected with an increase of internal sodium through opening of sodium channels, or with activation of other membrane sodium-transporting systems.

Animals↗
PubMed1975

[Bioelectrical characteristics of the membrane of identified Coretus corneus mollusk neurons A and B upon activation and blocking of the electrogenic sodium pump].

Activation of the electrogenic sodium pump by means of increasing concentration of intracellular sodium ions in identified neurons A and B of the mollusc was followed by the hyperpolarization, decrease of the excitability, and depression of the neurons rhythmic activity. Apart from that, the amplitude and the maximal rates of rise of ascending (VB) and descending (VH) phases of action potential (AP) were almost unchanged. The depression of the electrogenic sodium pump activity due to 2,4-DNP and potassium-free medium, led to the depolarization, increase of excitability and frequency of the rhythmic activity, and decrease of AP, VB, and VH. The decrease and increase of the excitability may be explained by the changes of the critical level of depolarization. The decrease of AP, VB and VH may be accounted for by the changes of time parameters of activation and inactivation of sodium and potassium channels which are characteristic for the depolarization effect.

Action Potentials↗
PubMed1983

Changes in the number and activity of sodium pumps in erythrocytes from patients with hyperthyroidism.

1. The sodium content, the rate and rate constant of ouabain-sensitive sodium efflux and the number of sodium pumps (indicated by the ouabain-binding capacity) were measured in erythrocytes from patients with hyperthyroidism and compared with values obtained in euthyroid patients and healthy control subjects. Erythrocyte zinc content was measured as a simple estimate of the content of carbonic anhydrase. 2. In the hyperthyroid patients, erythrocyte sodium content was increased, whereas the rate and rate constant of ouabain-sensitive sodium efflux, the ouabain-binding capacity and erythrocyte zinc content were all decreased. 3. The sodium pumps in hyperthyroidism had the same affinity for ouabain and the same rate constant per pump as those in healthy controls. 4. The decrease in the efflux rate constant could be entirely accounted for by the decrease in the number of sodium pumps. 5. Although the sodium efflux was decreased in the hyperthyroid patients, the change was less than expected for the decrease in the efflux rate constant. This suggests that there is an increase in the ground permeability of the erythrocyte membrane in hyperthyroidism. 6. In the hyperthyroid patients the number of sodium pumps and erythrocyte zinc content were inversely related to the plasma levels of thyroxine and tri-iodothyronine, but more closely to the latter. 7. These results suggest that the thyroid hormones may influence the erythrocyte's content of a range of proteins which happens to include the sodium pump.

Adult↗
PubMed1984

Effect of the serum concentration of the growth medium on the sodium pump site density of cultured HeLa cells.

The density of sodium pump sites in the plasma membrane of cultured HeLa cells has been measured as a function of the serum concentration of the cell growth medium. Growth in media containing increased concentrations of serum (from 1 to 20% v/v) leads to an increase in sodium pump site numbers (as measured by the specific binding of [3H]ouabain) and pump activity (as measured by the ouabain-sensitive 86Rb influx). Time-course studies show that (1) new sodium pump sites first appear some 3-6 h after transfer to medium containing an elevated serum concentration and (2) the serum-mediated increase in new sodium pump sites is completely abolished by the protein synthesis inhibitors, cycloheximide and actinomycin D. These results suggest that de novo protein synthesis is required for the development of the serum response. Preliminary characterization of the serum factor responsible for initiating the synthesis of new sodium pump sites indicates that the activity is associated with a high molecular weight serum fraction (greater than 50000). The different types of interaction seen between the serum effect and other experimental manoeuvres which initiate the synthesis of new pump sites (growth in low-K+ medium, growth in Li+ medium and pre-treatment with exogenous ATP) suggest that there may be more than one pathway for the control of sodium pump site synthesis in cultured HeLa cells.

Binding Sites↗
PubMed1990

The sodium pump needs its beta subunit.

The sodium pump Na,K-ATPase, located in the plasma membrane of all animal cells, is a member of a family of ion-translocating ATPases that share highly homologous catalytic subunits. In this family, only Na,K-ATPase has been established to be a heterodimer of catalytic (alpha) and glycoprotein (beta) subunits. The beta subunit has not been associated with the pump's transport or enzymatic activity, and its role in Na,K-ATPase function has been, until recently, a puzzle. In this review we describe what is known about the structure of beta and summarize evidence that expression of both alpha and beta subunits is required for Na,K-ATPase activity, that inhibition of glycosylation causes a decrease in accumulation of both alpha and beta subunits, and we provide evidence that pretranslational up-regulation of beta alone can lead to increased abundance of sodium pumps. These findings are all consistent with the hypothesis that the beta subunit regulates, through assembly of alpha beta heterodimers, the number of sodium pumps transported to the plasma membrane.

Animals↗
PubMed1997

Tissue-specific regulation of the sodium pump in DOCA-salt hypertension.

Alterations in sodium pump activity have been associated with volume-sensitive hypertension, but little is known regarding the molecular regulation of the catalytically active alpha-subunit of the sodium pump in these models. We examined changes in the mRNA abundance of the alpha-isoforms in tissues that might participate in sodium and volume regulation in the deoxycorticosterone acetate (DOCA)-high salt rat model. These tissues included kidney, heart, aorta, pituitary, and hypothalamus. This study assessed alterations arising from changes in dietary salt intake alone, from DOCA administration alone, and those requiring both DOCA and high salt with their attendant volume expansion and hypertension. Increased sodium intake produced no significant change in any isoform in the five tissues studied. DOCA administered with a low salt diet produced no significant change in any of the alpha-isoforms in any of the tissues studied. The combination of DOCA and high salt (HS), on the other hand, brought about a twofold increase in renal alpha1-mRNA abundance compared with control (alpha1, CTL: 101.1 +/- 9.3, DOCA-HS: 197.3 +/- 22.9, P < .0001). DOCA-HS also induced a marked increase in both alpha1- and alpha2-mRNA in the aorta (alpha1, CTL: 122.5 +/- 33.3 v DOCA-HS: 487.2 +/- 59.9, P = .001; alpha2, CTL: 126.6 +/- 40.0 v DOCA-HS: 559.8 +/- 271.7, P = .01). In contrast DOCA-HS animals showed a significant reduction in the alpha2-, but not alpha1-, mRNA abundance in heart (alpha2, CTL: 118.0 +/- 11.7 v DOCA-HS: 61.1 +/- 9.1, P = .006). No change was observed in pituitary or hypothalamus with DOCA-HS. Of factors known to modulate the mRNA abundance of the sodium pump, only the putative endogenous sodium pump inhibitor might account for the changes in the aorta and kidney. Reductions in aldosterone or hypertension might reduce alpha2 in the heart. Only the renal response would favor sodium reabsorption, which could contribute to the hypertensive process.

Animals↗
PubMed1993

Glutamate up-regulates alpha 1 and alpha 2 subunits of the sodium pump in astrocytes of mixed telencephalic cultures but not in pure astrocyte cultures.

Prior work employing an in vitro model of the cerebral cortex has shown that sodium pump activity is a critical determinant for neuronal survival of glutamate stimulation. We have hypothesized that up-regulation of total brain sodium pump activity will protect against potential excitotoxins. Increased sodium pump activity could theoretically occur by changes in the reaction rate (short-term) and/or by increased levels of sodium pump protein (long-term) and is potentially complex since the three catalytic (a) subunit isoforms of the sodium pump are distributed in a highly variable, cell-specific pattern in the brain. Short-term regulation (seconds to minutes) has been well studied: brain sodium pump exhibits a large dynamic range. In contrast, the possibility of long-term modulation of sodium pump activity has not been extensively explored. We used isoform specific antibodies and [3H]ouabain binding to determine whether prolonged stimulation of sodium pump activity in rodent telencephalic cultures increased total sodium pump enzyme. Exposure of mixed neuronal-glial cultures to high levels of glutamate (10 mM) for 18 h, which is highly toxic to neurons, was associated with an approximately 80% increase in alpha 1 and alpha 2 subunit expression by glia. Induction of alpha 2 subunit immunoreactivity was also associated with comparable changes in [3H]ouabain binding, suggesting that the up-regulation corresponded to functional alpha 2 protein. Shorter (30 min) glutamate treatments, which also killed neurons, did not produce similar changes in sodium pump expression. In contrast to mixed cultures, pure astrocyte cultures had undetectable alpha 2 and alpha 3 and moderate levels of alpha 1 protein, as confirmed by low levels of [3H]ouabain binding. Glutamate treatment using this protocol was associated with a decrease in alpha 1 sodium pump expression. We conclude that long-term regulation of the sodium pump can be demonstrated in glia which have developed in the presence of neurons. Both alpha 1 and alpha 2 isoforms of the sodium pump are involved in this response to glutamate.

Animals↗
PubMed1986

Myocardial sodium pump activity in endotoxin shock.

The effect of endotoxin administration on the integrity of sodium pump was studied in canine heart myocardium. Sodium pump activity was determined based on the 86Rb+ uptake by ventricular muscle strips. The results show that 4 hr following endotoxin administration the ouabain-sensitive 86Rb+ uptake was inhibited by 44-70%, and the inhibition was noncompetitive with 86Rb+ ions and was independent of Na+ concentrations. The sensitivity of sodium pump toward verapamil inhibition was unaffected by endotoxin administration, suggesting that the endotoxin-induced decrease in sodium pump activity is not mediated through alteration in either calcium or slow sodium channel. The sensitivity of 86Rb+ uptake to ouabain inhibition was decreased approximately sixfold in endotoxin-injected dogs. These data suggest that sodium pump is greatly impaired in dog hearts 4 hr after endotoxin administration. The impairment in sodium pump might have physiological significance in the development of myocardial dysfunction during endotoxic shock.

Animals↗
PubMed1980

The effects of vanadate on the fluxes of sodium and potassium ions through the sodium pump.

1. The effects of sodium orthovanadate on the fluxes of sodium and potassium (or rubidium) ions through the sodium pump have been investigated in intact human red cells and in resealed ghosts prepared from them. Sodium-potassium exchange, potassium-potassium exchange, pump reversal, sodium-sodium exchange and uncoupled sodium efflux have each been studied.2. When intact human red cells were incubated in high-sodium media containing vanadate in low concentrations, inhibition of potassium or rubidium influx was marked only if the potassium or rubidium concentration in the medium was sufficiently high to cause nearly maximal influx in the absence of vanadate. The absence of inhibition at lower potassium or rubidium concentrations cannot be explained by supposing that the onset of inhibition by vanadate is slower in these conditions.3. Lowering the extracellular sodium concentration, or raising the vanadate concentration, decreased the minimum concentration of extracellular potassium or rubidium at which inhibition by vanadate was detected.4. Experiments on potassium influx into intact red cells treated with the ionophore A23187 showed that magnesium ions act at intracellular sites to promote inhibition by vanadate.5. Measurements of potassium efflux from intact red cells incubated in high-sodium media, with or without potassium, showed that potassium-potassium exchange was inhibited by vanadate at low concentrations whereas reversal of the pump was not.6. Measurements of sodium efflux from intact red cells or resealed ghosts incubated in high-sodium media, with or without potassium, showed that vanadate had little or no effect on sodium-sodium exchange at concentrations at which sodium-potassium exchange was markedly reduced. Much higher concentrations of vanadate did cause partial inhibition of sodium-sodium exchange.7. Experiments to determine whether vanadate in low concentrations inhibited uncoupled sodium efflux were inconclusive, but suggested that the flux was inhibited. Measurements of the ATP hydrolysis that is thought to be associated with the uncoupled sodium efflux showed that this hydrolysis was strongly inhibited.8. The different effects of vanadate on the different fluxes are discussed, and related to the way in which vanadate is thought to act on the sodium pump.

Biological Transport, Active↗
PubMed2004

Subunit-specific coordinate upregulation of sodium pump activity in alveolar epithelial cells by lentivirus-mediated gene transfer.

Resolution of alveolar edema depends on active ion transport by sodium pumps located on the basolateral surface of alveolar epithelial cells (AECs), suggesting that upregulation of sodium pump activity may facilitate clearance of edema fluid. We have investigated the use of lentiviral vectors to augment sodium pump activity via gene transfer of sodium pump subunits to AECs. Full-length cDNA for the alpha(1) or beta(1) subunit of rat Na(+),K(+)-ATPase was cloned into the lentiviral vector pRRLsin.hCMV.IRES.EGFP. Rat AECs in primary culture were transduced on day 4 with lentiviral vectors pseudotyped with vesicular stomatitis virus glycoprotein G. Transduction with lentiviral vectors encoding either alpha(1) subunit (Lenti-alpha(1)-EGFP) or beta(1) subunit (Lenti-beta(1)-EGFP) led to dose-dependent increases in mRNA and protein for the corresponding subunit. Transduction with Lenti-beta(1)-EGFP was accompanied by coordinate upregulation of endogenous alpha(1) expression, whereas endogenous beta(1) expression was unchanged after transduction with Lenti-alpha(1)-EGFP. Consistent with these findings, transduction with Lenti-beta(1)-EGFP, but not Lenti-alpha(1)-EGFP, led to augmentation of sodium pump activity as a result of increases in Na(+),K(+)-ATPase holoenzyme. Sodium pump alpha(2) subunit and sodium channel protein did not change after Lenti-beta(1)-EGFP transduction. These results demonstrate that overall sodium pump activity can be efficiently upregulated in AECs specifically via gene transfer of the sodium pump beta(1) subunit and support the feasibility of lentivirus-mediated gene transfer to augment alveolar fluid clearance.

Animals↗
PubMed1989

Erythrocyte sodium pump activity in bipolar affective disorder and other psychiatric disorders.

Erythrocyte ouabain-inhibitable sodium pump activity, a measure of NaK-ATPase activity, was studied in 6 diagnostic groups of psychiatric subjects: bipolar affective disorder, unipolar depressive disorder, neurotic depression, chronic alcohol abuse, schizoaffective disorder, and schizophrenia, and in sex- and age-matched normal controls. In the bipolar manic-depressive group, which was restricted to lithium-free subjects, values for sodium pump activity were significantly lower than in the controls (-11.4%, n = 53, p less than 0.001); subgrouping of the bipolar group by sex or age showed a significantly lower sodium pump activity in each of the groups. In the unipolar depressive group, values for sodium pump activity were significantly higher than in the controls (+13.7%, n = 12, p less than 0.01). The difference in direction of changed sodium pump activity between the bipolar and the unipolar groups was also observed in the values for subgroups of subjects in the two categories who were in a depressed state at the time the blood sample was taken. In the chronic alcohol abuse group, values for sodium pump activity were significantly higher than those for the control group (+13.5%, n = 20, p less than 0.05). In the neurotic depression (n = 24), schizoaffective (n = 12), and schizophrenia (n = 35) groups, there were no significant differences in sodium pump activity between the group of psychiatric subjects and their matched controls. These observations indicate that there is a trait-dependent deficiency of NaK-ATPase activity in bipolar affective disorder.

Adolescent↗
PubMed1987

Electrophysiological evidence for ammonium as a substitute for potassium in activating the sodium pump in a crayfish sensory neuron.

Electrophysiological studies were performed on slowly adapting cells of the crayfish (Astacus astacus) stretch receptor to examine some aspects of the operation of the sodium pump. Intracellular sodium activity (aiNa) and pH (pHi) were measured with liquid ion exchanger microelectrodes and the effects of NH3/NH+4 were observed. In cells in which the sodium pump was inhibited by K+-free solution, NH+4 induced a decrease of aiNa that can be explained only in Na+ extrusion is assumed. pHi measurements provide indirect evidence that NH+4 was taken up at the same time as Na+ was extruded. Ouabain blocks the operation of the sodium pump in the presence of K+ and NH+4. This result suggests that the ammonium-mediated decrease in aiNa in K+-free solution was caused by activation of the sodium pump. The results obtained by electrophysiological methods in a living cell are qualitatively in good agreement when compared with biochemical investigations on assays of crustacean Na+-K+ ATPase.

Ammonia↗