Red blood cell Na+ content is poorly related to essential hypertension and to membrane Na+ transport abnormalities.
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Biological Transport↗
Biomedical subjects
R Garay
Publications and source records attributed to R Garay.
[Beneficial effects of xipamide on pH and Ca2+ ions of cardiac cells].
We have shown that xipamide is the only antihypertensive agent able to selectively inhibit the anion exchanger (AE), a transport system translocating (i) chloride and bicarbonate (thus participating to internal pH), but also (ii) Na+ as NaCO3-(which could explain the natriuretic effect of xipamide). On the other hand, Ollivier (Val de Grâce, Paris) has shown that xipamide exerts a beneficial action on heart by favoring left ventricular relaxation in essential hypertensive patients exhibiting cardiac hypertrophy. In order to understand this clinical effect, we have studied the effect of xipamide on pH and cytosolic free calcium in cultured Rat cardiocytes (H9c2 line). pHi was measured at equilibrium using 14C-DMO and cytosolic free calcium was measured spectrofluorimetrically with Fura2 (Shimadzu RF 5000). 1) The presence of bicarbonate induced a 0.39 +/- 0.14 (mean +/- SD; n = 3) alkalinization; final pHi was 7.08 +/- 0.15 (n = 8). Nor 20 microM DIDS (specific AE inhibitor), neither 50 microM xipamide were able to modify this result. This suggests that the alkalinization is not due to the anion exchanger. 2) After preincubation in the presence of 0.5 microM DIDS, we observed a 0.35 +/- 0.21 acidification (n = 4). Conversely, 0.5 microM xipamide induced a 0.22 +/- 0.16 alkalinization (n = 4). 3) Xipamide (0.5-500 microM) increased the internal K/Na ratio (at 0.5 microM, delta = 3.1 +/- 0.2; n = 3); this was mainly due to internal K+ increase.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Kinetic study of the Ca2+ pump in erythrocytes from essential hypertensive patients.
Ca2+ pump kinetics were investigated in erythrocytes from 22 essential hypertensive patients and 20 normotensive controls (under initial-rate and steady-state conditions, using Sr2+ as a Ca2+ analogue). The mean value of the apparent dissociation constant for total internal Ca2+ (KCa) was slightly but significantly increased in the hypertensive population (73 +/- 7 versus 55 +/- 3 mumol/l cells, mean +/- s.e.m., P = 0.042 Mann-Whitney U-test). The statistical analysis showed that this was due to six essential hypertensives who exhibited a dissociation constant for Ca2+ that was higher than the upper 95% normal confidence limit (KCa = 116 +/- 7 mumol/l cells), and abnormally high maximal pump rates (7.7 +/- 0.6 versus 5.0 +/- 0.2 mmol/l cells per h in normotensives, P less than 0.001). In addition, the apparent dissociation constant for Ca2+ was inversely correlated with plasma renin activity, although the correlation was only borderline (P = 0.076). In the remaining 16 hypertensive patients, all kinetic parameters of the Ca2+ pump were within the normal range. Finally, a simultaneous study of Na+ transport kinetics suggested that erythrocyte Ca2+ and Na+ transport abnormalities were independent phenomena. Our results do not support the concept that primary hypertension (as a whole entity) is associated with a ubiquitous defect in the plasma membrane Ca2+ pump. However, in some essential hypertensive patients (about 25%) the erythrocyte Ca2+ pump exhibited an apparent decreased affinity for internal Ca2+. A similar defect in vascular smooth muscle may induce a delayed Ca2+ extrusion after the opening of Ca2+ channels, a disturbance likely to be translated into increased vascular reactivity.
Adenosine Triphosphate↗
Evidence for a major route for zinc uptake in human red blood cells: [Zn(HCO3)2Cl]- influx through the [Cl-/HCO3-] anion exchanger.
The initial rate of Zn2+ uptake in human red cells was measured by atomic absorption. A very important fraction of Zn2+ uptake was inhibited by DIDS with IC50 = 0.3 microM (and by furosemide and bumetanide with IC50 of 200 and 500 microM, respectively). DIDS-sensitive Zn2+ uptake exhibited the following properties: 1) It required the simultaneous presence of both external HCO3- and Cl-. 2) In Cl- containing media, it was strongly stimulated by external HCO3- following a sigmoidal (S-shaped) and saturable function, which was fitted by a Hanes equation, with n = 2 and an apparent dissociation constant (for external HCO3-) of 5.3 +/- 0.9 mM (mean +/- SD of four experiments). The maximal rate of Zn2+ uptake at saturating HCO3- concentrations was 50.7 +/- 4.8 mmol (liter cells x h)-1. 3) In HCO3- containing media, it was strongly stimulated by external Cl- following a Michaelis-like equation with an apparent dissociation constant (for external Cl-) of 88 +/- 11 mM (mean +/- SD of three experiments). 4) Bicarbonate-stimulated Zn2+ uptake was inhibited by physiological concentrations of phosphate (sulfate was a much less potent inhibitor than phosphate). A kinetic analysis of the data strongly suggested that zinc was transported by the anion carrier in the form of the monovalent anion complex: [Zn(HCO3)2Cl]-.
Bicarbonates↗
Inhibitory action of norepinephrine on sodium transport in vascular smooth muscle cells in culture.
Cultured vascular smooth muscle cells from porcine aortas incubated in Na+ -free medium rapidly release their intracellular Na+ contents (Nai) (23 +/- 4% of baseline after 60 min incubation, mean +/- SEM of 18 experiments). Total Nai release was inhibited by 35-40% after addition of ouabain and by 60-70% after addition of ouabain + bumetanide. Norepinephrine inhibited ouabain and bumetanide-sensitives Na+ efflux with an IC50 of about 10(-9)-10(-8) M. Addition of the alpha-adrenergic agonist phenylephrine (10 microM) to the cells mimicked the inhibitory action of norepinephrine on Nai release. Conversely, the beta-adrenergic agonist isoproterenol was without effect on Nai release. Simultaneous addition of 10 microM norepinephrine and the alpha-adrenergic antagonist phentolamine prevented any effect of norepinephrine on the rate of Nai decline. In A-10 cultured vascular smooth muscle cells, the alpha-adrenergic agonist phenylephrine (10 microM) inhibited 40.0 +/- 8.1% of ouabain-sensitive Rb+ influx and 70.7 +/- 6.9% of bumetanide-sensitive Rb+ influx (mean +/- SEM of three experiments). 50% inhibition of bumetanide-sensitive Rb+ influx was obtained with about 5 x 10(-7) M of phenylephrine. Our results show that in vascular smooth muscle cells a [Na+, K+, Cl-]-cotransport system is able to catalyze outward Na+ movements (in Na+ -free media) of a similar order of magnitude to those of the Na+, K+ pump and that alpha-adrenergic stimulation markedly inhibits Na+ efflux (and Rb+ influx) through these two transport systems.
Animals↗
Stimulation of Na(+)-H+ exchange, the Na(+)-K+ pump and Na+,K+,Cl- cotransport by endothelin-1 in cultured vascular smooth muscle cells.
Endothelin-1 concentrations higher than 10(-10) mol/l were able to strongly stimulate Na(+)-H+ exchange, the Na(+)-K+ pump and the Na+,K+Cl- cotransport system in A10 vascular smooth muscle cells. The stimulation of Na(+)-H+ exchange was more marked in fresh than in H(+)-loaded cells, suggesting an increase in the apparent affinity for internal H+. Pump stimulation appeared to be secondary to sodium entry through Na(+)-H+ exchange because it was absent in (1) Na(+)-loaded cells and (2) in the presence of ethyl-isopropylamiloride (EIPA). Stimulation of cotransport was blocked by indomethacin, suggesting the involvement of a cyclo-oxygenase product. In conclusion, the action of endothelin-1 in vascular smooth muscle induces the onset of negative feedback mechanisms which enhance the ability of the vascular cells to regulate disturbances in Na+,K+ and Cl- contents.
Biological Transport↗
A mechanical stress increases sodium ion content in vascular smooth muscle cells through a calcium-dependent pathway: prevention by cicletanine via a cyclo-oxygenase product.
The non-laminar (rather turbulent) flow induced by cell washings was able to reversibly increase the sodium ion (Na+) content in cultured A10 aortic smooth muscle cells. Similar changes, although to a lesser extent, were observed in cardiocytes but not in fibroblasts, erythrocytes, thymocytes or macrophages, suggesting that the changes are specific to excitable cells. The increase in vascular sodium content had the following properties: (1) It was inhibited by nitrendipine; (2) it was accompanied by an increase in the free cytosolic Ca2+ content; (3) it was unable to stimulate the sodium pump; and (4) it reflected the qualitative and quantitative composition of the incubation media. These observations suggested that a non-laminar flow is able to open potential-dependent calcium channels, with secondary internalization of high amounts of extracellular ions. These ionic perturbations were blocked by low concentrations of cicletanine; the half-maximal inhibitory concentration (IC50) was about 10(-9) mol/l on internal sodium. The protective effects of cicletanine were inhibited by indomethacin, suggesting that they are mediated by a cyclooxygenase metabolite, perhaps prostacyclin. Captopril and diuretic drugs such as hydrochlorothiazide, furosemide, spironolactone or acetazolamide were unable to protect vascular cells against the harmful effects of cell washings.
Animals↗
Stimulation of the Na+, K+ pump and the (Na+, K+, Cl-) cotransport system by endothelin-1 in cultured vascular smooth muscle cells: involvement of cyclo-oxygenase products.
The effect of endothelin (ET-1) on vascular smooth muscle cell Na+ and K+ regulation was studied in the A10 cultured cell line. In contrast with other vasoconstrictors, ET-1 was able to strongly stimulate both the Na+, K+ pump and the (Na+, K+, Cl-) cotransport system at concentrations higher than 10(-10) M. This did not appear to reflect a direct interaction with the transport proteins because ET-1 was without effect on the same transport systems in human red cells. Indomethacin, at concentrations of 10(-5) M, was able to counteract the pump and cotransport stimulation by ET-1. These results suggest that the potent vasoconstrictive action of ET-1 induces a negative feedback mechanism via a cyclo-oxygenase product, which enhances the ability of vascular smooth muscle cells to regulate Na+ and K+ contents.
Biological Transport, Active↗
Reduction of membrane band 7 and activation of volume stimulated (K+, Cl-)-cotransport in a case of congenital stomatocytosis.
We report on a case of congenital stomatocytosis in a French boy presenting with a haemolytic anaemia requiring splenectomy at the age of 6. The red cells included 15-20% stomatocytes and displayed a marked increase of volume. Their osmotic resistance and density were reduced; however, their deformability was unaltered in isotonicity. Erythrocyte Na+ was high (27 mEq/l) and K+ low (65 mEq/l). The newly described (K+, Cl-)-cotransporter normally triggered by hypo-osmotic stress, was activated to maximal capacity. Membrane band 7 was reduced by 72%. From anamnestic data, the condition appears to have been transmitted by the father. The mother proved to be strictly normal on clinical, morphological, osmotic and biochemical bases. We suggest that the partly missing band 7 may play an important role in the genesis of stomatocytosis.
Anemia, Hemolytic, Congenital↗
[Ionic perturbations produced by a non-laminar flow in vascular smooth muscle cells in culture. Protection by cicletanine via a cyclo-oxygenase metabolite].
The non-laminar (rather turbulent) flow, induced by cell washings was able to reversibly increase internal Na+ contents in cultured aortic smooth muscle (A10 cells). Similar changes (although to a lesser extent) were observed in cardiocytes but not in fibroblasts, erythrocytes, thymocytes or macrophages, suggesting that they are specific for excitable cells. The increased vascular sodium content had the following properties: it was inhibited by nitrendipine; it was accompanied by an increase in free cytosolic Ca2 contents; it was unable to stimulate the sodium pump and (iv) it reflected the qualitative and quantitative composition of the incubation media. These observations suggested to us that the increased vascular sodium content results from the opening of potential-dependent calcium channels with secondary internalisation of high amounts of extracellular ions. The ionic perturbations were blocked by low concentrations of cicletanine (IC50 of about 10(-9) M on intracellular sodium). Moreover, the protective effects of cicletanine were inhibited by indomethacin, suggesting that they are mediated by a cyclo-oxygenase metabolite, perhaps prostacyclin. Sodium nitroprusside, a compound able to stimulate calcium entry in the sarcoplasmic reticulum via cyclic GMP, was also able to protect vascular cells (although it acted at higher concentrations than cicletanine). Conversely, captopril and diuretic drugs such as hydrochlorothiazide, furosemide, spironolactone and acetazolamide were unable to protect vascular cells against the deleterious effects of cell washings.
Antihypertensive Agents↗
[Decrease in the regulatory capacity of the calcium pump in a subgroup of essential hypertensive patients].
We developed a new flux technique, useful for the clinical investigation of Ca2+ pump kinetics in intact erythrocytes. The initial rate of Sr2+ efflux (mediated by the Ca2+ pump) was studied as a function of steady state erythrocyte Sr2+ and Ca2+ contents in 22 Caucasian essential hypertensive patients (8 females, 14 males), aged 39-66 years (mean 51) and compared with 20 normotensive control subjects (10 females, 10 males), aged 22-57 years (mean 41). Kinetic analysis of the data (by using a two-sites model) allowed the determination of the apparent dissociation constants for internal Ca2+ (KCa) and for internal Sr2+ (KSr) and the maximal rate of Sr2+ efflux (Vmax). Mean values of these kinetic parameters were slightly increased in the hypertensive population. However, only the increase in KCa reached statistical significance (73 +/- 7 vs 55 +/- 3 mumol/l.cells, Mann-Whitney U test; p = 0.042). Individual analysis of the data showed that 6 essential hypertensives had a KCa higher than the upper normal limit (95 p. 100 confidence limit) of the normotensive group. In addition, mean values of Vmax and KSr were also significantly higher in these six essential hypertensives. In conclusion, about 25 p. 100 of the hypertensive patients had a decreased apparent affinity of the Ca2+ pump for internal Ca2+, which appears to be compensated (in the basal state) by an increased maximal pump rate. A similar abnormality in vascular smooth muscle cells may induce increased contractility by transitory cell Ca2+ retention after the opening of Ca2+ channels.
Adult↗
[Therapeutic response to canrenone of patients with essential hypertension as a function of sodium transport anomalies and ouabain sensitivity of erythrocytes].
The presence of Na+ transport abnormalities (decreased affinity of the Na+/K+ pump or the Na+, K+ cotransport for internal Na+, increased Na+:Li+ countertransport, increased Na+ leak), Na+ content, Na+/K+ pump activity and sensitivity to ouabain were investigated in erythrocytes from 13 patients with essential hypertension. According to the presence or absence of Na+ transport abnormalities, the patients were divided into two groups: TrNa(+) (n = 9) and TrNa(-) (n = 4) respectively. Compared with TrNa(-) patients, TrNa(+) patients were characterized by: (i) a higher arterial pressure (131.4 +/- 11.8 vs 110.0 +/- 13.2 mmHg, p less than 0.05), (ii) an increased erythrocyte Na+ content (8.9 +/- 1.0 vs 6.3 +/- 0.8 mmol/l.cells, p less than 0.01) associated with (iii) a decreased rate constant of Na+/K+ pump activity (235 +/- 26 vs 309 +/- 45 h-1, p less than 0.05) and (iv) a higher sensitivity to ouabain (0.76 +/- 0.23 vs 1.12 +/- 0.26 microM, p less than 0.05). Oral administration of canrenone 50 mg per day during 7 weeks decreased mean arterial pressure by 10-30 mmHg in 6 out of the 9 TrNa(+) patients. Conversely, it decreased mean arterial pressure in only one out of the 4 TrNa(-) patients. The hypotensive effect of canrenone in TrNa(+) patients was not associated with normalization of their Na+/K+ pump activity. Canrenone did not modify the sensitivity to ouabain of either the TrNa(+) or the TrNa(-) patients. Before treatment, acute injection of ouabain provoked an inhibition of the erythrocyte Na+/K+ pump, without any change in Na+ content.(ABSTRACT TRUNCATED AT 250 WORDS)
Biological Transport↗
Correlation between total and free magnesium levels in human red blood cells. Influence of HLA antigens.
Total and free magnesium contents were determined by atomic absorption spectrophotometry and 31P nuclear magnetic resonance on red blood cells of healthy blood donors of known HLA groups. A statistically significant correlation was found between free and total magnesium contents (r = 0.67, P less than 0.02). The previously described low total magnesium contents in HLA-B35+ subjects were associated with low free Mg2+ contents. Therefore, total and free magnesium and HLA-associated genetic factors are closely related.
Erythrocytes↗
Demonstration of a Na+: Mg2+ exchange in human red cells by its sensitivity to tricyclic antidepressant drugs.
Iminodibenzyl-, iminostilbene-, dibenzocycloheptadiene-, dibenzooxepine- and dibenzothiepine-derivatives of tricyclic antidepressant drugs were able to inhibit Na+-stimulated Mg2+ efflux in human erythrocytes at concentrations of 10(-5) -10(-3) mol/l. Tricyclic antidepressant drugs belonging to other chemical groups, non-tricyclic antidepressant drugs and phenothiazines were less potent inhibitors (IC50 of 10(-4) mol/l or higher). Imipramine and dothiepine, the most potent compounds, inhibited the Mg2+ carrier with IC50 of 2.5 and 4 x 10(-5) mol/l respectively. These IC50 are of similar order of magnitude to those of some classical transport inhibitors (such as furosemide for the [Na+ K+, Cl-]-cotransport system). In addition, these concentrations of imipramine and dothiepine were free of: i) side effects on other erythrocyte Na+ and K+ transport pathways (with the exception of a slight inhibition of Ca2+-sensitive K+-channels and [Na+,K+,Cl-]- and [K+,Cl-]-cotransport systems) and ii) toxic effects on the membrane leak for divalent or monovalent cations. Therefore, we selected imipramine as an useful tool for investigating fluxes catalyzed by the Na+-stimulated Mg2+ carrier. Imipramine was tested on the initial rate of ouabain and bumetanide-resistant net Na+ influx in Na+-depleted, Mg2+-loaded erythrocytes. The compound was able to inhibit a Na+ influx of about 300-500 mumol (1.cells x h)-1 with an IC50 of about 3 x 10(-5) mol/l. This imipramine-sensitive Na+ influx was coupled with an imipramine-sensitive Mg2+ efflux in a stoichiometry of 3.03 +/- 0.34 (mean +/- SEM of 7 experiments).
Antidepressive Agents, Tricyclic↗
A study of the interaction between the Na+, K+ pump and Na+:Ca2+ exchange in macrophages and vascular smooth muscle cells.
Blaustein (Am J Physiol 1977;232:C165-C173) postulated that Na+:Ca2+ exchange in vascular smooth muscle plays a key role in the link between sodium and hypertension. Investigation of this hypothesis was facilitated by the use of: a) Sr2+, a slowly transported Ca2+ analogue, and b) new quasispecific inhibitors of Na+:Ca2+ exchange such as 2',4'-dimethylbenzamil. Preliminary experiments in mouse macrophages showed that the initial rate of Sr2+ uptake lasted for at least 15 minutes and was therefore easier to measure than the initial rate of unidirectional isotopic Ca2+ influx (which lasted less than 30 seconds). In cells with normal Na+ content, basal Sr2+ influx (432 +/- 77 mumol [L cells X h]-1; mean +/- SEM of seven experiments) exhibited properties compatible with a ground membrane leak for divalent cations (quasilinear dependence on the external Sr2+ concentration, partial or full resistance to external Ca2+, Ba2+, verapamil, and 2',4'-dimethylbenzamil). Membrane depolarization by external K+ was unable to modify basal Sr2+ uptake. Conversely, a 100% increase in cell Na+ content by preincubation with ouabain increased the rate of Sr2+ uptake by 233 +/- 48 mumol (L cells X h)-1 (mean +/- SEM of seven experiments). 2',4'-Dimethylbenzamil, but not the Ca2+ antagonists diltiazem or methoxyverapamil, inhibited ouabain-stimulated Sr2+ influx (IC50 of about 3 X 10(-5) M). 2',4'-Dimethylbenzamil was also able to inhibit Na+ efflux (by 3.05 +/- 0.98 mmol (L cells X h)-1; mean +/- SEM of three experiments) suggesting the existence of Na+:Sr2+ exchange.(ABSTRACT TRUNCATED AT 250 WORDS)
Amiloride↗
Antihypertensive effect of canrenone in a model where endogenous ouabain-like factors are present.
The effect of canrenone, an antialdosterone and partial ouabain-agonist drug, was studied in rats that developed volume expansion and hypertension after renal mass reduction and excess Na+ intake (RRM-salt). The RRM-salt was characterized by: (1) increased endogenous "digitalis-like" compounds in plasma [cross reactivity with digoxin-antibodies (57.5 +/- 5.0 vs. 42.1 +/- 3.8 pg/ml, p less than 0.02); inhibition of kidney Na+, K+-ATPase activity (135 +/- 5 vs. 154 +/- 5 mumol/mg/h, p less than 0.01); and inhibition of Na+ extrusion from normal erythrocytes (5.96 +/- 0.40 vs. 7.68 +/- 0.34 mmol/L cells/h, p less than 0.01)]; (2) reduced Na+, K+-pump activity (7.34 +/- 0.29 vs. 10.88 +/- 0.41 mmol/L cells/h, p less than 0.001) and increased Na+ content (4.66 +/- .08 vs. 4.16 +/- 0.11 mmol/L cells, p less than 0.01) in erythrocytes; and (3) low plasma renin activity (2.1 +/- 0.9 vs. 12.6 +/- 1.6 ng/ml/h). Ninety minutes after the administration to RRM-salt of a single oral dose of 60 mg/kg of canrenone, the systolic blood pressure decreased by 36 +/- 4 mm Hg (mean +/- SEM). Chronic canrenone administration (60 mg/kg/day) resulted in a marked antihypertensive effect associated to a correction of volume expansion, a decrease in endogenous "digitalis-like" compounds, and a partial recovery of Na+, K+-pump activity and Na+ content in erythrocytes. Our results suggest that the antihypertensive effect in RRM-salt rats results, at least in part, from antagonism with endogenous "digitalis-like" compounds.
Animals↗
High sensitivity of the Na+, K+-pump of human red blood cells to genins of cardiac glycosides.
1. Four different cardiac glycosides (ouabain, digitoxin, digoxin and gitoxin) and their corresponding genins were tested on Na+, K+-pump fluxes measured under steady-state and initial rate conditions (non equilibrium conditions) in human and rat erythrocytes and in mouse macrophages. 2. In human red cells, Na+, K+-pump fluxes exhibited up to 8 fold higher sensitivity to genins than to glycosides. In addition genins, but not the corresponding glycosides, exhibited double reactivity with regard to the erythrocyte Na+, K+-pump (with the exception of gitoxigenin). A weak reactivity component was similar to the one of the corresponding glycosides (IC50 of about 10(-6) M) and a high reactivity component exhibited IC50 values varying from 0.1 to 0.5 X 10(-6) M for digitoxigenin and ouabagenin respectively. 3. In contrast with human red cells, the initial rate of Na+, K+-pump fluxes in rat erythrocytes and mouse macrophages was less sensitive to genins than to the corresponding cardiac glycosides. 4. Dihydroouabain was 3, 10 and 75 times less active than ouabain in inhibiting the initial rate of Na+, K+-pump fluxes in human and rat erythrocytes and in mouse macrophages respectively. 5. In conclusion, Na+, K+-pump fluxes measured under initial rate conditions in human erythrocytes exhibit an unusually high sensitivity to genins of cardiac glycosides. This property probably results from the fast binding rate constants of genins and the slow association rates of glycosides to human red cells.
Animals↗
Disturbances in Na+ transport systems induced by ethanol in human red blood cells.
The effects of ethanol on fluxes catalyzed by four Na+ transport systems (ouabain-sensitive Na+, K+ pump, bumetanide-sensitive Na+, K+ cotransport system, Na+:Li+- countertransport and anion carrier) and on Na+ and K+ leaks were investigated in human red blood cells. Ethanol concentrations higher than 32 mM were required in order to significantly modify erythrocyte Na+ transport function. The observed changes can be summarized as follows: (a) stimulation of Na+ efflux through the Na+, K+ pump (by 21-32% at 160-400 mM) and Na+:Li+ countertransport (by 34-59% at 160-400 mM); (b) inhibition of outward Na+, K+ cotransport (by 23-34% at 160-400 mM) and LiCO3- influx through the anion carrier (by 17-21% at 64-400 mM); and (c) increase in Na+ and K+ leaks (by 13-16% at 64-400 mM). The effects of ethanol on the Na+,K+ pump and Na+,K+ cotransport system resulted from changes in maximal rates of Na+ efflux (increased and decreased, respectively) without any significant effect on the apparent affinities for internal Na+. Erythrocytes preincubated for 1 hr with 160 mM ethanol, washed and further incubated in flux media, recovered a normal Na+ transport function. In conclusion, high concentrations of ethanol induced reversible perturbations of fluxes catalyzed by erythrocyte Na+ transport systems. The observed effects may reflect disturbances in Na+ transport function associated with severe intoxication.
Biological Transport, Active↗