Ethanol predominantly alters sodium influx in human leucocytes

1990 ◽  
Vol 78 (2) ◽  
pp. 235-238 ◽  
Author(s):  
J. Main ◽  
T. Thomas
Keyword(s):  
Sodium Transport ◽  
Sodium Pump ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Exact Nature ◽  
Sodium Influx ◽  
Pump Activity

1. Although ethanol appears to alter cellular sodium transport, the exact nature of its effects has not been clearly defined. We have studied the effects of different concentrations of ethanol on human leucocyte sodium content, and on the rise in leucocyte sodium content which occurs during sodium pump blockade with ouabain. 2. Sodium content was significantly reduced after a 20 min incubation with ethanol at concentrations between 17 and 170 mmol/l. 3. The rise in sodium content during a 20 min incubation with ouabain was significantly less in the presence of 170 mmol/l ethanol as compared with 17 mmol/l ethanol. 4. These results suggest that the effect of ethanol on intracellular sodium content is independent of sodium pump activity, i.e. it is mediated through reduced sodium influx.

Studies of Sodium Transport in Thymocytes of Rats with DOC/Salt Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 65s-67s ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton
Keyword(s):  
Rate Constant ◽  
Sodium Transport ◽  
Dry Weight ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Control Group ◽  
Efflux Rate ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Efflux Rate Constant

1. Sodium transport and intracellular sodium content were studied in thymocytes of rats made hypertensive by treatment for 4 or 8 weeks with deoxycorticosterone (DOC) and salt (DOC/salt). 2. The systolic blood pressure in the DOC/salt animals was 152 ± sem 3 and 189 ± 3 mmHg after 4 and 8 weeks' treatment respectively. This was significantly higher than pressures in their respective controls (124 ± 4 and 126 ± 5 mmHg), which had been given 1% sodium chloride solution (171 mmol/l) only. 3. The total sodium efflux rate constant in the DOC/salt rats was lower than that in the control group after 8 weeks of treatment (5.56 ± sem 0.21 vs 6.12 ± 0.11 h−1; P < 0.05) but not after 4 weeks of treatment (5.93 ± 0.13 vs 6.32 ± 0.13 h−1;0.1 > P > 0.05). 4. Intracellular sodium content in the DOC/salt rats was significantly higher than that of the control animals after 8 weeks' treatment (49.6 ± 2.5 vs 42.1 ± 1.0 mmol/kg dry weight; P < 0.05). 5. No significant changes were observed in intracellular potassium content, sodium influx or ouabain-insensitive sodium efflux rate constant.

Relationship between plasma growth hormone concentration and cellular sodium transport in acromegaly

1992 ◽  
Vol 127 (1) ◽  
pp. 38-43 ◽  
Author(s):  
Hans Herlitz ◽  
Olof Jonsson ◽  
Bengt-Åke Bengtsson
Keyword(s):  
Growth Hormone ◽  
Sodium Transport ◽  
Negative Relationship ◽  
Sodium Content ◽  
Plasma Growth Hormone ◽  
Sodium Influx ◽  
Active Acromegaly ◽  
One Year ◽  
Plasma Gh

We investigated the relationship between mean plasma growth hormone (GH) concentration and cellular sodium transport in untreated and treated acromegaly. Seventeen patients (age 55±3 years) with active acromegaly were studied with respect to plasma GH (mean of 24 h GH profile) and erythrocyte electrolyte content as well as transmembrane sodium transport. The patients were reinvestigated two weeks after successful surgery (N=14) and again after one year (N=13). Erythrocyte electrolytes were analyzed by flame photometry and sodium influx and efflux rate constant determined by in vitro incubation using a modified Keyne's formula. In patients with active acromegaly there was a significant positive correlation between IGF-1 and cellular sodium transport, while GH tended to show a negative relationship to the same parameter. After successful treatment, both IGF-1 and GH disclosed a positive relationship to cellular sodium transport. After one year, a significant increase in erythrocyte sodium content was seen in the patients compared to the preoperative situation. In conclusion, if this is a generalized phenomenon the results are compatible with a sodium-retaining effect of GH via stimulation of transmembrane sodium transport. In active acromegaly this may be counteracted by a sodium transport inhibitor giving the reverse relationship between GH and cellular sodium transport.

Effect of Zinc on Leucocyte Sodium Transport In Vitro

1978 ◽  
Vol 54 (5) ◽  
pp. 585-587 ◽  
Author(s):  
J. Patrick ◽  
J. Michael ◽  
M. N. Golden ◽  
B. E. Golden ◽  
P. J. Hilton
Keyword(s):  
Tissue Culture ◽  
Sodium Transport ◽  
Zinc Concentration ◽  
Culture Fluid ◽  
Sodium Content ◽  
Cell Water ◽  
Sodium Influx ◽  
Sodium Efflux

1. In a preparation of human leucocytes maintained in tissue culture fluid, increasing the extracellular zinc concentration leads to a significant increase in both ouabain-sensitive sodium efflux and in sodium influx. 2. Cell water and sodium content do not alter significantly with increasing extracellular zinc concentration. 3. A small increase in the ouabain-insensitive sodium efflux can be demonstrated when the external zinc concentration is raised from 0·75 μmol/l to 90 μmol/l.

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

1990 ◽  
Vol 258 (1) ◽  
pp. C24-C29 ◽  
Author(s):  
B. J. Cohen ◽  
C. Lechene
Keyword(s):  
Initial Rate ◽  
Rat Hepatocytes ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Cell Swelling ◽  
Hypotonic Solution ◽  
Potassium Efflux ◽  
Pump Rate ◽  
Pump Activity ◽  
Stimulation Of

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

Effect of the Calcium Antagonist Verapamil on Human Leucocyte Sodium Transport in vitro

1985 ◽  
Vol 68 (2) ◽  
pp. 239-241 ◽  
Author(s):  
H. H. Gray ◽  
L. Poston ◽  
V. E. Johnson ◽  
P. J. Hilton
Keyword(s):  
Essential Hypertension ◽  
Calcium Antagonist ◽  
Sodium Transport ◽  
Rate Constants ◽  
Sodium Pump ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Pump Activity ◽  
External Calcium

1. Sodium efflux rate constants and intracellular sodium were measured in leucocytes from healthy volunteers in the presence and absence of the calcium antagonist verapamil hydrochloride. 2. Verapamil stimulated sodium pump activity and this effect was dependent on the presence of external calcium. 3. Verapamil has been reported to reverse the abnormality of sodium transport seen in leucocytes from patients with essential hypertension and the present study demonstrates that sodium pump activity in leucocytes from control subjects is also stimulated by exposure to verapamil in vitro. This direct cellular effect appears to be due to the calcium antagonist properties of the drug.

NMR measurements of intracellular sodium in the rabbit proximal tubule

1985 ◽  
Vol 249 (1) ◽  
pp. F160-F168 ◽  
Author(s):  
S. R. Gullans ◽  
M. J. Avison ◽  
T. Ogino ◽  
G. Giebisch ◽  
R. G. Shulman
Keyword(s):  
Time Course ◽  
Cell Membranes ◽  
Sodium Content ◽  
Shift Reagent ◽  
Intracellular Sodium ◽  
Dependent Manner ◽  
Extracellular Medium ◽  
Sodium Influx ◽  
Sodium Permeability ◽  
Triton X

The present study evaluated the use of nuclear magnetic resonance (NMR) spectroscopy to monitor directly and continuously intracellular sodium levels in rabbit renal cortical tubule suspensions. When the paramagnetic shift reagent dysprosium tripolyphosphate was added to the extracellular medium it was possible to resolve signals from intracellular and extracellular sodium without adversely affecting cellular viability. An efflux of intracellular sodium against a significant concentration gradient was observed when sodium-loaded cells were warmed from 4 to 37 degrees C. At 37 degrees C in steady state, inhibition of Na+-K+-ATPase activity by ouabain increased intracellular sodium content in a dose-dependent and time-dependent manner. A biphasic time course of increased intracellular sodium following ouabain (10(-3) M) suggested that the sodium permeability of the plasma membrane may decrease following pump inhibition, thus limiting sodium influx. Nystatin, an agent known to facilitate sodium entry across cell membranes, increased intracellular sodium fivefold. In another series of experiments several maneuvers were performed to ascertain the fraction of intracellular sodium that was NMR visible. Quantitative assessment of either an efflux or influx of sodium indicated that the NMR visibility of the transported sodium was 100%. Furthermore, disruption of the cell membranes with Triton X-100 showed that the entire pool of intracellular sodium was 100% NMR visible.(ABSTRACT TRUNCATED AT 250 WORDS)

Erratum

1970 ◽  
Vol 52 (2) ◽  
pp. 494-494
Keyword(s):  
Fresh Water ◽  
Sodium Transport ◽  
Sodium Concentration ◽  
Sodium Influx ◽  
Lampetra Planeri

MORRIS, R. & BULL, J. M. Studies on fresh water osmoregulation in the Ammocoete larvae of Lampetra planeri Bloch. III. The effect of external and internal sodium concentration on sodium transport. J. Exp. Biol. 52, 2, pp. 275-290. Page 287. Figure 5. For ‘Sodium influx (µM/gm./hr.)’ read ‘Sodium influx (µM/3gm./hr.)’

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