Branchial Sodium Transport Mechanisms in Scyliorhinus Canicula: Evidence for Na+/NH4+ and Na+ H+ Exchanges and for A Role of Carbonic Anhydrase

1973 ◽  
Vol 58 (2) ◽  
pp. 487-502
Author(s):  
P. PAYAN
Keyword(s):  
Sodium Transport ◽  
Ammonia Excretion ◽  
Inhibitory Effect ◽  
The Body ◽  
Control Fish ◽  
Transport Mechanisms ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Sodium Uptake ◽  
Scyliorhinus Canicula

1. Branchial sodium exchanges were measured with the help of 24Na in the marine elasmobranch Scyliorhinus canicula. Handling causes a transient increase of the sodium influx and decrease of the sodium efflux in both intact and hypophysectomized fish. 2. Ammonia-loading (300 µ-equiv./100 g) is followed by an increase of both influx and efflux of sodium resulting in an augmented net sodium uptake lasting for at least 4 h. Ammonia excretion is also increased but only for 2 h. Ammonia-loading results in a metabolic acidosis lasting for at least 4 h. 3. HCl injection (100 µ-equiv./100 g) produces an increase of both influx and efflux of sodium resulting in an augmented net sodium uptake lasting for at least 4 h. Ammonia excretion is not affected. 4. Acetazolamide injection (10 mg/100 g) results in a depression of the sodium influx, while the sodium efflux remains unchanged. This inhibitory effect is observed in control fish as well as in fish treated with HCl or ammonium salt injections. 5. These observations confirm that the gill plays a major role in the maintenance of the pH of the body fluids. The similarities between the sodium transport mechanisms of Scyliorhinus and of the freshwater teleosts are emphasized. These results suggest that living elasmobranchs may have retained branchial mechanisms inherited from their freshwater ancestors.

Branchial Sodium Exchange and Ammonia Excretion in the Goldfish Carassius Auratus. Effects of Ammonia-Loading and Temperature Changes

1972 ◽  
Vol 56 (3) ◽  
pp. 601-620 ◽  
Author(s):  
J. MAETZ
Keyword(s):  
Carassius Auratus ◽  
Chloride Concentration ◽  
Ammonia Excretion ◽  
Effect Of Temperature ◽  
Control Fish ◽  
Sodium Balance ◽  
Ammonium Ions ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Net Uptake

1. Sodium influx and efflux and ammonia excretion by the gill have been studied as a function of external sodium chloride concentration in Carassius auratus before and after loading the fish with ammonia. 2. No correlation between net sodium uptake and ammonia excretion is observed, either when the net uptake changes with an external sodium change or when net uptake increases with ammonia-loading. Branchial handling of chlroide ions cannot explain this absence of correlation. 3. Comparison of the concentrations of free base ammonia (NH3) and of ammonium ions (NH4+) in both (dorsal aorta) and external medium at the end of the closed-circuit experiments on control or ammonia-loaded fish demonstrates that the gill is permeable to the ionized form of ammonia. 4. An abrupt temperature decrease (16 → 6 °C) affects the sodium influx (Q10 = 3) much more than the sodium efflux (Q10 = 1.7). Sodium balance becomes negative unless the fish is ammonia-loaded. The observed effects of temperature are reversible when the fish is returned to 16 °C. Branchial ammonia excretion is highly temperature-sensitive (Q10 = 4) in control fish when metabolic production limits ammonia excretion. After ammonia-loading, when most of the ammonia cleared by the gill is exogenous, the effect of temperature on branchial permeability to ammonia (Q10 = 1.9) suggests a passive transfer of ammonium ions. 5. The contributors of the kidney and the gill in sodium loss and ammonia excretion are compared in intact and ammonia-loaded fish.

Abstract 087: Human Stomach Cell Gastrin Inhibits Renal NHE3 and NaKATPase in Concert With the Renal D1R

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
John J Gildea ◽  
Peng Xu ◽  
Chi Zhang ◽  
Dora Bigler Wang ◽  
Hahn T Tran ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Human Colon ◽  
Inhibitory Effect ◽  
Human Stomach ◽  
D1 Receptor ◽  
The Body ◽  
Human Colon Cancer ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Renal Proximal Tubule Cells

The digestive track secretes gastrin in response to sodium ingestion stimulating increased renal sodium excretion. We previously showed that gastrin secreted by human colon cancer cells (SW626) can bind to cell surface cholecystokinin receptors on renal proximal tubule cells (RPTC), modulating the natriuretic dopaminergic system. We tested the hypothesis that a similar gastro/renal axis exists in humans. Novel human stomach antrum G-cell lines from 6 separate individuals were isolated and each shown to express gastrin mRNA and protein, and bind Phaseolus vulgaris Leucoagglutinin (PHA-l) by fluorescence lectin affinity (marker for gastrin secreting cells). It was determined that the D1 receptor (D1R) is also found on G-Cells. In human stomach tissue, gastrin expression was increased by Fenofibrate treatment, (PPARα agonist, p= 0.07, in 3 live ex-vivo cultured human stomachs). Moreover, we tested the effect of gastrin on CCKB2 receptors in human RPTC. Gastrin (100 nM 15 min.) increased RPTC phospholipace-C (PLC) activity by 1.07± 0.01 fold, N=35, p<0.0001, using a PLC-FRET biosensor, CYPHR, but did not increase cAMP levels using the specific cAMP-FRET biosensor, ICUE-YR. Both gastrin and SKF83822 (100 nM, a cAMP specific D1R agonist, 15 min) alone reduced sodium influx into RPTC via NHE3 (from VEH 100± 4.7% to 73.5± 6.2% or 74.1± 4.3% respectively N=6, p<0.05), but gastrin along with SKF83822 decreased sodium influx more than either alone (57.2 ± 5.8% N=6, p<0.05). Sodium efflux via NaKATPase was reduced by SKF83822 (from VEH 100± 3.9% to 84.2± 3.3%, N=6, p<0.05), but not gastrin alone, however SKF83822 along with gastrin reduced sodium efflux more than SKF83822 alone (72.3±5.1% vs N=6, p<0.05). Additionally we found that Angiotensin II (AngII, 10 nM, 15 min.) increased NHE3 activity (12.3± 3.6% N=6, p<0.01) and this increase was completely blocked by gastrin (N=6, p<0.01). The PLC inhibitor U73122 reversed the inhibitory effect of gastrin on NHE3 and NaKATPase. Gastrin was also found to decrease the amount of fluorescent AngII binding to RPTCs (27.4± 6.1% N=6, p<0.01) and this decrease was completely blocked by U73122. Thus, both stomach gastrin and the renal D1R inhibit NHE3 and NaKATPase, to increase sodium elimination from the body after salt is ingested.

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.

scholarly journals The Effect of External Sodium and Calcium Concentrations on Sodium Fluxes by Salt-Depleted and Non-Depleted Minnows, Phoxinus Phoxinus (L.)

1987 ◽  
Vol 131 (1) ◽  
pp. 417-425
Author(s):  
W. J. FRAIN
Keyword(s):  
Sodium Concentration ◽  
Uptake Mechanism ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Sodium Uptake ◽  
Km Value ◽  
Concentration Changes ◽  
The Relationship ◽  
Very High ◽  
External Calcium

The relationship between sodium influx and external sodium concentration in Phoxinus is complex and unusual. In non-depleted fish the relationship is approximately that given by the Michaelis-Menten equation of enzyme kinetics. However, the Km value (a measure of the affinity of the sodium uptake mechanism for sodium) is very high (3mmoll−1), indicating a low affinity of the uptake mechanism for sodium. On sodium depletion, the relationship between sodium influx and external sodium concentration changes to produce a curve which has a stepped appearance, and is unusual in that the maximum influx is not increased above that in non-depleted fish. The overall Km alters very little; however, the Km for the lower part of the curve is very low (0.05 mmoll−1). A model is proposed to explain these results in the form of two sodium uptake mechanisms working in parallel across the gill. The second carrier is only active when the fish is sodium-depleted and kept in low external sodium concentrations. Neither the external sodium concentration nor the external calcium concentration has any direct effect on sodium efflux. However, fish depleted in 1 mmoll−1 calcium have a lower sodium efflux than fish depleted in distilled water. Calcium appears to reduce the permeability of the gill to ions such as sodium. Since calcium has no effect on sodium influx, changes in gill permeability do not involve the sodium influxmechanism.

The Involvement of Sodium Transport in the Volume Regulation of the Amphipod Crustacean, Gammarus Duebeni

1970 ◽  
Vol 53 (3) ◽  
pp. 737-751
Author(s):  
A. P. M. LOCKWOOD
Keyword(s):  
Blood Concentration ◽  
Volume Regulation ◽  
Evolutionary Significance ◽  
Fluid Loss ◽  
Body Volume ◽  
Transport Mechanisms ◽  
Sodium Influx ◽  
Sodium Uptake ◽  
Subsequent Decrease ◽  
Amphipod Crustacean

1. The effect on sodium influx of reduction in the fluid volume of the amphipod Gammarus duebeni has been investigated. 2. Removal of water and sodium by exposure to isotonic sucrose or mannitol results in no significant change in blood concentration but is followed subsequently by a marked increase in sodium influx. 3. The increased influx is due, at least in part, to increased active uptake of sodium. 4. Physical removal of blood by pipette stimulates a greater degree of increased uptake in some individuals by comparison with the controls. For technical reasons the increases as measured are smaller than in §2 above and in some individuals there is no response. 5. When the blood concentration is caused to rise at the same time as body volume is reduced there is subsequent decrease in sodium influx. 6. It is concluded that a mechanism is present which initiates an increase in sodium uptake on reduction of blood volume. This mechanism may be of value in replacing fluid loss resulting from haemorrhage, if water uptake accompanies sodium uptake. 7. The evolutionary significance of such a mechanism is discussed in relation to development of active transport mechanisms in present-day freshwater and brackish-water forms.

Sodium Regulation in the Fresh-Water Amphipod, Gammarus Pulex (L.)

1967 ◽  
Vol 46 (3) ◽  
pp. 499-518
Author(s):  
D. W. SUTCLIFFE
Keyword(s):  
Fresh Water ◽  
Body Surface ◽  
Loss Rate ◽  
Sodium Concentration ◽  
The Body ◽  
Uptake Mechanism ◽  
Sodium Influx ◽  
Sodium Uptake ◽  
Sodium Loss ◽  
Total Sodium

1. Sodium influx and loss rates in Gammarus pulex were measured at constant temperatures. The sodium loss rate was immediately influenced by a change in temperature, with a Q10 of 1.5 to 2.0 at temperatures between 0.3 and 21.5° C. The sodium influx rate is apparently influenced in the same way. 2. The sodium uptake mechanism in G. pulex from three localities was half-saturated at an external concentration of 0.10-0.15 mM/l. sodium. 3. The total sodium loss rate remained approximately constant in animals acclimatized to the range of external concentrations from 2 to about 0.2 mM/l. sodium. 18% of the sodium was lost in urine with a sodium concentration estimated at 30-50 mM/l. The remainder of the sodium loss was due to diffusion across the body surface. 4. In animals acclimatized to concentrations below about 0.2 mM/l. sodium the sodium loss rate was reduced, due to (a) a lower diffusion rate following a fall in the blood sodium concentration, and (b) the elaboration of a more dilute urine. 5. There was a very close association between changes in the blood sodium concentration, the elaboration of a very dilute urine, and the rate of sodium uptake at the body surface. The results indicate that a fall in the blood sodium concentration leads to simultaneous activation of the sodium uptake mechanisms at the body surface and in the antennary glands. 6. It is estimated that, by producing a dilute urine, total sodium uptake in G. pulex is shared equally between the renal uptake mechanism and the mechanism situated at the body surface. 7. In sea-water media G. pulex drinks and expels fluid from the gut. In a medium slightly hyperosmotic to the normal blood concentration the amount imbibed was equal to the normal rate of urine flow when in fresh water.

Active Transport and Sodium Fluxes at Moult in the Amphipod, Gammarus Duebeni

1969 ◽  
Vol 51 (3) ◽  
pp. 591-605
Author(s):  
A. P. M. LOCKWOOD ◽  
W. R. H. ANDREWS
Keyword(s):  
Fresh Water ◽  
Body Surface ◽  
Major Part ◽  
Sea Water ◽  
Sucrose Solution ◽  
The Body ◽  
Active Sodium ◽  
Sodium Influx ◽  
Sodium Uptake ◽  
High Level

1. The sodium fluxes of individual Gammarus duebeni, which moulted in sea water, have been followed daily from the morning following moult for at least 6 days. 2. Sodium influx from sea water declined from 15.1µM/animal/hr. on the first morning after moult to 1.7µM/animal/hr. by the tenth day after moult. 3. Sodium influx from 10 mM/l. NaCl plus sucrose solution isotonic with sea water declines from 4.48µM/animal/hr. to 0.14µM/animal/hr. in inter-moult animals. 4. Thionine inhibits over 90% of the influx from 10 mM/l NaCl plus isotonic sucrose on the first day after moult, and this, together with other evidence, suggests that the major part of the influx from this medium is due to active sodium uptake. The rate of active uptake is comparable with, or faster than, the rate of uptake by animals acclimatized to fresh water. 5. The influx occurs primarily across the body surface. It is suggested that the high level of sodium uptake is associated with the water uptake which occurs at moult.

A Passive Sodium Transport Inhibitory Factor (Inhibitin) Released from Leukaemic Promyelocytes in Culture

1984 ◽  
Vol 66 (3) ◽  
pp. 365-368
Author(s):  
Kevin Morgan ◽  
M. Afzal Mir
Keyword(s):  
Rate Constant ◽  
Sodium Transport ◽  
Culture Media ◽  
Inhibitory Effect ◽  
Inhibitory Factor ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Stable Factor ◽  
Heat Stable ◽  
Efflux Rate Constant

1. Previous studies have shown that myeloid leukaemic blast cells contain a heat stable factor which inhibits bidirectional sodium transport in normal erythrocytes. This study was undertaken to establish whether leukaemic promyelocytes in culture secrete this factor. 2. Two cell-lines of leukaemic promyelocytes (HL-60 and JR) were grown and culture media from both reduced significantly the ouabain-insensitive sodium efflux rate constant, whereas conditioned culture medium (incubated like the cells in culture) had no inhibitory effect. 3. Promyelocyte extract reduced significantly (P < 0.01) the total sodium efflux rate constant from 0.393 ± 0.030 (sd) to 0.311 ± 0.060, and ouabain-insensitive efflux rate constant from 0.131 ± 0.008 to 0.079 ± 0.009 (P<0.001). 4. The inhibitory factor was heat stable (80°C for 30 min) and it inhibited sodium efflux through a pathway which was not inhibited by ouabain or frusemide. 5. These studies suggest that leukaemic promyelocytes secrete the previously identified passive sodium transport inhibitory factor.

Altered Membrane Sodium Transport and the Presence of a Plasma Ouabain-Like Inhibitory Factor in Acute Myeloid Leukaemia

1975 ◽  
Vol 48 (3) ◽  
pp. 213-218
Author(s):  
M. Afzal Mir ◽  
H. Bobinski
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Sodium Transport ◽  
Normal Subjects ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
High Sodium ◽  
Electrolyte Disturbances ◽  
Similar Factor ◽  
Acute Myeloid

1. Sodium transport studies were performed in erythrocytes from normal subjects and from patients with acute myeloid leukaemia. Sodium influx and efflux rates were increased in erythrocytes from leukaemic patients. 2. The ouabain-sensitive component of sodium efflux was increased in leukaemic erythrocytes. 3. The high sodium efflux from leukaemic erythrocytes was decreased when the incubation media contained leukaemic plasma, suggesting the presence of an ouabain-like factor in the plasma. Paired experiments failed to show the presence of a similar factor in normal plasma. 4. Leukaemic erythrocytes showed a significantly greater ouabain uptake than the normal cells. 5. The results are discussed in relation to the widespread electrolyte disturbances in acute myeloid leukaemia.

Changes of sodium transport in erythrocytes of the maturing rabbit

1975 ◽  
Vol 228 (2) ◽  
pp. 461-464 ◽  
Author(s):  
EK Smith ◽  
L Weihrauch ◽  
D Farrington
Keyword(s):  
Atpase Activity ◽  
Sodium Transport ◽  
Sodium Concentration ◽  
Red Cells ◽  
Potassium Content ◽  
High Potassium ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Low Sodium ◽  
Total Sodium

The red blood cells of New Zealand white rabbits have a low sodium and high potassium content. As the animals mature, the sodium concentration rises and the potassium content falls; studies of red cells from a group of five young and five mature animals revealed a highly significant increase of cell sodium with age that was associated with a significant fall in the rate of ouabain-inhibited active sodium efflux. This difference was still seen when the sodium concentration within the cells from old and young animals was equalized and elevated to saturating levels for active pump efflux. Total sodium efflux, however, increased significantly with age as did total sodium influx so that a steady state was reached. Ouabain-sensitive ATPase activity fell significantly in the cell membranes from older animals and ouabain-insensitive ATPase increased with age. The survival time of 51Cr-labeled red cells was significantly longer in old than in young animals and it is concluded that as the rabbit matures its red cells survive for a longer period and this is associated with the changes of sodium transport and ATPase activity that have been documented.

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