DIRECT MEASUREMENT OF SODIUM UPTAKE BY TOAD BLADDER MUCOSAL CELLS

1972 ◽  
Vol 55 (1) ◽  
pp. 195-201 ◽  
Author(s):  
D. R. FERGUSON ◽  
M. W. SMITH
Keyword(s):  
Direct Measurement ◽  
Direct Evidence ◽  
Sodium Concentration ◽  
Mucosal Surface ◽  
Toad Bladder ◽  
Contact Period ◽  
Simple Diffusion ◽  
Sodium Uptake ◽  
Low Concentrations ◽  
Mucosal Cells

SUMMARY A technique is described by which the unidirectional influx of sodium into toad bladder mucosal cells can be measured over short periods. The uptake of sodium, which is linear over a 60 s contact period, changes in a non-linear way when the external sodium concentration is varied from 5 to 115mm. Vasotocin applied to the serosal surface increases significantly the influx of sodium; amiloride applied to the mucosal surface inhibits influx. This is true whether high or low concentrations of sodium are used to bathe the mucosal surface. The kinetics for the unidirectional influx of sodium provide direct evidence that the passage of sodium into this tissue is by some means other than simple diffusion.

The effect of enternal sodium concentration upon sodium fluxes in Chironomus dorsalis (Meig.) and Camptochironomus tentans (Fabr.), and the effect of other ions on sodium influx in C. tentans

1975 ◽  
Vol 62 (1) ◽  
pp. 141-155
Author(s):  
DA Wright
Keyword(s):  
Steady State ◽  
Sodium Concentration ◽  
Fourth Instar ◽  
Half Maximum ◽  
Uptake Mechanism ◽  
Sodium Influx ◽  
Sodium Uptake ◽  
Low Concentrations ◽  
Salt Depletion

In comparison with other freshwater animals, the sodium uptake mechanism in fourth instar larvae of both C. tentans and C. dorsalis has a moderate affinity for sodium. In both species half maximum influx (Km) occurs at about 0.57 mM-Na+ and is unaltered by salt depletion. Maximum influx is achieved in steady-state C. tentans at 1.9 mM-Na+, and in steady-state C. dorsalis at 3.0 mM-Na+. Both of these values increase on depletion. Efflux also appears to be saturable at higher external sodium concentrations. In C. tentans, sodium may be transported independently of chloride, although it seems likely that sodium movement is enhanced by chloride. Sulphate strongly inhibits sodium influx. Nitrate apparently inhibits sodium influx at low concentrations, but this inhibition is progressively overcome at external sodium concentrations approaching 4 mM. A number of cations interfere with sodium influx in depleted C. tentans, notably H+, Li+ and, to a lesser extent NH4+. It is suggested that these ions compete with sodium for carrier sites. Potassium is apparently transported independently of sodium.

Sodium Regulation in the Freshwater Mollusc Limnaea Stagnalis (L.) (Gastropoda: Pulmonata)

1970 ◽  
Vol 53 (1) ◽  
pp. 147-163 ◽  
Author(s):  
PETER GREENAWAY
Keyword(s):  
Blood Volume ◽  
Tap Water ◽  
Sodium Concentration ◽  
Sodium Balance ◽  
Uptake Mechanism ◽  
Sodium Influx ◽  
Sodium Uptake ◽  
Limnaea Stagnalis ◽  
Total Body ◽  
Sodium Regulation

1. Sodium regulation in normal, sodium-depleted and blood-depleted snails has been investigated. 2. Limnaea stagnalis has a sodium uptake mechanism with a high affinity for sodium ions, near maximum influx occurring in external sodium concentrations of 1.5-2 mM-Na/l and half maximum influx at 0.25 mM-Na/l. 3. L. stagnalis can maintain sodium balance in media containing 0.025 mM-Na/l. Adaptation to this concentration is achieved mainly by an increased rate of sodium uptake and a fall of 37 % in blood sodium concentration, but also by a reduction of the sodium loss rate and a decrease in blood volume. 4. A loss of 23% of total body sodium is necessary to stimulate increased sodium uptake. This loss causes near maximal stimulation of the sodium uptake mechanism. 5. An experimentally induced reduction of blood volume in L. stagnalis increases sodium uptake to three times the normal level. 6. About 40% of sodium influx from artificial tap water containing 0.35 mM-Na/l into normal snails is due to an exchange component. Similar exchange components of sodium influx were also observed in sodium-depleted and blood-depleted snails in the same external sodium concentration.

Apical acidification induces paracellular injury in canine gastric mucosal monolayers

1994 ◽  
Vol 267 (6) ◽  
pp. G1012-G1020 ◽  
Author(s):  
M. C. Chen ◽  
A. Chang ◽  
T. Buhl ◽  
M. Tanner ◽  
A. H. Soll
Keyword(s):  
Short Circuit ◽  
Phase 1 ◽  
Short Circuit Current ◽  
Paracellular Permeability ◽  
Ussing Chambers ◽  
Low Concentrations ◽  
Three Phase ◽  
Mucosal Cells ◽  
Primary Monolayer ◽  
Primary Monolayer Cultures

We used primary monolayer cultures of enzyme-dispersed canine oxyntic mucosal cells mounted in Ussing chambers to characterize the apical barrier to H+. [3H]mannitol flux (MF) and [14C]inulin flux (IF) were used as size probes for tight junctions. Apical H+ produced a three-phase effect. In phase 1, as the apical pH was decreased from 7 to about 2.5, resistance (R) increased, but short-circuit current (Isc) did not change. In phase 2, an increased paracellular permeability developed at pH below 2.5-1.7, evidenced by decreased R and increased MF but not IF. Size sieving and monolayer integrity were preserved, and this paracellular leak was either fully reversed or stabilized by apical neutralization, depending on the duration of the paracellular leak. In phase 3, after sustained exposure to an apical pH below approximately 2, transepithelial integrity was lost; R decreased to fluid R, and both MF and IF increased. Basolateral acidification below pH 5.5 produced rapid monolayer disruption. Low concentrations of cytochalasin D (CD) decreased R and increased MF but not IF; apical acidification to pH 4 after CD increased R and decreased the MF, indicating reduced paracellular permeability by apical H+. Apical amiloride did not alter Isc; however, after 48 h of treatment with hydrocortisone and insulin, an amiloride-sensitive Isc component became evident. Our data indicate that the increase in R observed with apical acidification reflects decreased paracellular permeability and that the earliest injury with apical acidification is a selective paracellular leak.

scholarly journals The Site of the Stimulatory Action of Vasopressin on Sodium Transport in Toad Bladder

1968 ◽  
Vol 51 (5) ◽  
pp. 589-605 ◽  
Author(s):  
Mortimer M. Civan ◽  
Howard S. Frazier
Keyword(s):  
Sodium Transport ◽  
Direct Evidence ◽  
Ionic Mobility ◽  
Toad Bladder ◽  
Permeability Barrier ◽  
Total Resistance ◽  
Stimulatory Action ◽  
Resistance Change ◽  
Site Of Action ◽  
Mucosal Side

Vasopressin increases the net transport of sodium across the isolated urinary bladder of the toad by increasing the mobility of sodium ion within the tissue. This change is reflected in a decreased DC resistance of the bladder; identification of the permeability barrier which is affected localizes the site of action of vasopressin on sodium transport. Cells of the epithelial layer were impaled from the mucosal side with glass micropipettes while current pulses were passed through the bladder. The resulting voltage deflections across the bladder and between the micropipette and mucosal reference solution were proportional to the resistance across the entire bladder and across the mucosal or apical permeability barrier, respectively. The position of the exploring micropipette was not changed and vasopressin was added to the serosal medium. In 10 successful impalements, the apical permeability barrier contributed 54% of the initial total transbladder resistance, but 98% of the total resistance change following vasopressin occurred at this site. This finding provides direct evidence that vasopressin acts to increase ionic mobility selectively across the apical permeability barrier of the transporting cells of the toad bladder.

Efflux of sodium from isolated toad bladder

1963 ◽  
Vol 205 (4) ◽  
pp. 718-722 ◽  
Author(s):  
Howard S. Frazier ◽  
Earle I. Hammer
Keyword(s):  
Diffusion Process ◽  
Active Transport ◽  
Mucosal Surface ◽  
Toad Bladder ◽  
Surface Replacement ◽  
Abrupt Increase ◽  
Exchange Diffusion ◽  
Serosal Surface ◽  
Saturation Kinetics ◽  
Stimulation Of

A method of simultaneously determining the rates of loss of Na24 across the mucosal and serosal surfaces of the isolated toad bladder is described. The addition of vasopressin to the serosal medium causes an abrupt increase in the efflux of Na24 across the mucosal boundary, with no significant change in the efflux across the serosal surface. Replacement of sodium in the mucosal medium with choline causes no change in the efflux of Na24 across either the mucosal or serosal surfaces. The results indicate that the stimulation of active transport of sodium across the bladder after vasopressin is the result solely of an increase in the permeability to sodium of the mucosal surface. Vasopressin does not act directly on the active transport step at the serosal surface. In addition, the saturation kinetics which describe the process of sodium entry at the mucosal boundary are not the result of an exchange diffusion process, and appear not to be due to a sodium-induced change in the permeability of this surface to sodium.

scholarly journals Effect of Changes in Transepithelial Transport on the Uptake of Sodium across the Outer Surface of the Frog Skin

1971 ◽  
Vol 58 (2) ◽  
pp. 131-144 ◽  
Author(s):  
Thomas U. L. Biber
Keyword(s):  
Outer Surface ◽  
Frog Skin ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Sodium Concentration ◽  
Transepithelial Transport ◽  
Linear Component ◽  
Sodium Uptake

The unidirectional sodium, uptake at the outer surface of the frog skin was measured by the method described by Biber and Curran (8). With bathing solutions containing 6 mM NaCl there is a good correlation between sodium uptake and short-circuit current (SCC) measured simultaneously except that the average uptake is about 40% higher than the average SCC. The discrepancy between uptake and SCC increases approximately in proportion to an increase in sodium concentration of the bathing solutions. Amiloride inhibits the unidirectional sodium uptake by 21 and 69% at a sodium concentration of 115 and 6 mM, respectively. This indicates that amiloride acts on the entry step of sodium but additional effects cannot be excluded. The sodium, uptake is not affected by 10-4 M ouabain at a sodium concentration of 115 mM but is inhibited by 40% at a sodium concentration of 6 mM. Replacement of air by nitrogen leads to a 40% decrease of sodium uptake at a sodium concentration of 6 mM. The results support the view proposed previously (8) that the sodium uptake is made up of two components, a linear component which is, essentially, not involved in transepithelial movement of sodium and a saturating component which reflects changes in transepithelial transport. Amiloride, seems largely to affect the saturating component.

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.

scholarly journals Frontier mystery: An unusual mound of kopi mourning caps on the eastern edge of the Simpson Desert

2019 ◽  
Vol 22 ◽  
pp. 59-63 ◽  
Author(s):  
Giles Hamm ◽  
Don Rowlands ◽  
Mike Smith
Keyword(s):  
Direct Evidence ◽  
Contact Period ◽  
Single Event ◽  
Social Ranking ◽  
Dune Field ◽  
Colonial Expansion ◽  
Colonial Frontier ◽  
Eastern Edge ◽  
Simpson Desert ◽  
Single Cluster

On the eastern edge of the Simpson dune field, an unusual find of 40–60 mourning caps in a single cluster, prompts us to raise issues about its interpretation. This region is known for violence along the colonial frontier, and this kopi site is only one to two days walk from the site of a known massacre of a ceremonial gathering of people at Kaliduwarry waterhole in about 1878. There is no direct evidence showing that this site coincides with colonial expansion in this region in the late 1870s, but the condition of these caps and their geomorphic context indicate that this site cannot be older than a few hundred years. If it dates to the pre-contact period in the 1800s, this kopi site must reflect a higher degree of social ranking and complexity than is usually assumed in the ethnography. Whether or not this remarkable site relates to the death of a single, high-ranked individual or multiple deaths on the colonial frontier in a single event, this cluster of mourning caps indicates that 40–60 people were in mourning simultaneously.

A carrier-mediated system for transport of biotin in rat intestine in vitro

1987 ◽  
Vol 252 (1) ◽  
pp. G52-G55 ◽  
Author(s):  
H. M. Said ◽  
R. Redha
Keyword(s):  
Methyl Ester ◽  
Temperature Dependent ◽  
Rat Intestine ◽  
Simple Diffusion ◽  
Low Concentrations ◽  
Structural Analogues ◽  
High Concentrations ◽  
Biotin Molecule ◽  
Energy Dependent

Transport of biotin was examined in rat intestine using the everted sac technique. Transport of 0.1 microM biotin was linear with time for at least 30 min of incubation and occurred at a rate of 3.7 pmol X g initial tissue wet wt-1 X min-1. Transport of biotin was higher in the jejunum than the ileum and was minimum in the colon (85 +/- 6, 36 +/- 6, and 2.8 +/- 0.6 pmol X g initial tissue wet wt-1 X 25 min-1, respectively). In the jejunum, transport of biotin was saturable at low concentrations (Kt = 3.73, microM, Vmax = 3.11 nmol X g initial tissue wet wt-1 X 25 min-1) but linear at higher concentrations (greater than 10 microM). The transport of low concentrations of biotin was inhibited by structural analogues (desthiobiotin, biotin methyl ester, diaminobiotin, and biocytin), Na+ dependent, energy dependent, temperature dependent, and proceeded against a concentration gradient in the serosal compartment. No metabolic alteration occurs to the biotin molecule during transport. This study demonstrates that biotin transport in rat intestine occurs by a carrier-mediated process at low concentrations and by simple diffusion at high concentrations. Furthermore, the carrier-mediated process is Na+, energy, and temperature dependent.

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