scholarly journals Sodium chloride transport by rabbit gallbladder. Direct evidence for a coupled NaCl influx process.

1975 ◽  
Vol 65 (6) ◽  
pp. 769-795 ◽  
Author(s):  
R A Frizzell ◽  
M C Dugas ◽  
S G Schultz

The results of the present study that NaCl transport by in vitro rabbit gallbladder must be a consequence of a neutral coupled carrier-mediated mechanism that ultimately results in the active absorption of both ions; pure electrical coupling between the movements of Na and Cl can be excluded on the grounds of electrphysiologic considerations. Studies on the unidirectional influxes of Na and Cl have localized the site of this coupled mechanism to the mucosal membranes. Studies on the intracellular ion concentrations and the intracellular electrical potential are consistent with the notion that (a) the coupled NaCl influx process results in the movement of Cl from the mucosal solution into the cell against an apparent electrochemical potential difference; (b) the energy for the uphill movement of Cl is derived from the Na gradient across the mucosal membrane which is maintained by an active Na extrusion mechanism located at the basolateral membranes; and (c) Cl exit from the cell across the basolateral membranes is directed down an electrochemical potential gradient and may be diffusional. Finally, as for the case of rabbit ileum, the coupled NaCl influx process is inhibited by elevated intracellular levels of cyclic 3',5'-adenosine monophosphate. A working model for transcellular and paracellular NaCl transport by in vitro rabbit gallbladder is proposed.

1975 ◽  
Vol 228 (6) ◽  
pp. 1808-1814 ◽  
Author(s):  
HN Nellans ◽  
RA Frizzell ◽  
SG Schultz

Acetazolamide (8 mM) aboishes active Cl absorption and inhibits but does not abolish active Na absorption by stripped, short-circuited rabbit ileum. These effects are not accompanied by significant changes in the transmural electrical potential difference or short-circuit current. Studies of the undirectional influxes of Na andCl indicate that acetazolamide inhibits the neutral, coupled NaCl influx process at the mucosal membranes. This action appears to explain the observed effect of acetazolamide on active, transepithelial Na and Cl transport. Acetazolamide did not significantly inhibit either spontaneous or theophylline-induced Cl secretion by this preparation, suggesting that the theophylline-induced secretion may not simply be due tothe unmasking of a preexisting efflux process when the neutral influx mechanism is inhibited by theophylline. Finally, inhibition of the neutral NaCl influx process by acetazolamide does not appear to be attributable to an inhibition of endogenous HCO3production or an elevation in intracellular cyclic-AMP levels. Instead, it appearstheat the effect of acetazolamide is due to a direct interaction with a membrane component involved in the coupled influx process.


1964 ◽  
Vol 48 (2) ◽  
pp. 375-378 ◽  
Author(s):  
Stanley G. Schultz ◽  
Ralph Zalusky ◽  
Arthur E. Gass

Unidirectional Cl fluxes across in vitro segments of rabbit ileum have been determined both in the absence and in the presence of an electrochemical potential gradient. The results indicate that Cl transport in this preparation can be attributed to purely passive forces uninfluenced by solvent drag or exchange diffusion. Furthermore, on the basis of this and previous studies, it has been demonstrated that the sum of the partial ionic conductances of Na and Cl accounts for at least 90 per cent of the total tissue conductance.


1989 ◽  
Vol 77 (2) ◽  
pp. 161-166 ◽  
Author(s):  
K. J. Moriarty ◽  
N. B. Higgs ◽  
M. Woodford ◽  
L. A. Turnberg

1. Cholera toxin stimulates intestinal secretion in vitro by activation of mucosal adenylate cyclase. However, it has been proposed that cholera toxin promotes secretion in vivo mainly through an indirect mechanism involving enteric neural reflexes. 2. We examined this hypothesis further by studying the influence of neuronal blockade on cholera toxin-induced changes in fluid transport across rabbit ileum in vitro. Mucosa, stripped of muscle layers, was mounted in flux chambers and luminal application of crude cholera toxin (2 μg/ml) caused a delayed but sustained rise in the short-circuit current, electrical potential difference and Cl− secretion. Pretreatment with the nerve-blocking drug, tetrodotoxin (5 × 10−6 mol/l serosal side), failed to influence the secretory response to cholera toxin, and addition of tetrodotoxin at the peak response to cholera toxin also had no effect. 3. That tetrodotoxin could block neurally mediated secretagogues was confirmed by the demonstration that the electrical responses to neurotensin (10−7 mol/l and 10−8 mol/l) were blocked by tetrodotoxin (5 × 10−6 mol/l). Furthermore, the response to cholera toxin of segments of ileum, which included the myenteric, submucosal and mucosal nerve plexuses, was not inhibited by tetrodotoxin. 4. We conclude that cholera toxin-induced secretion in rabbit ileum in vitro is not mediated via a neurological mechanism.


1984 ◽  
Vol 247 (1) ◽  
pp. C3-C9 ◽  
Author(s):  
J. Bijman ◽  
P. M. Quinton

Parameters of electrolyte transport in single sweat glands in normal subjects and cystic fibrosis (CF) patients were monitored and compared. Results indicate that in both normal and CF sweat ducts, Na+ is reabsorbed by an active process in which Cl- follows passively while K+ is secreted. However, while net NaCl reabsorption is markedly lower, the electrical potential associated with sweat emerging from the sweat duct is significantly more negative in CF than in normal subjects. Comparison of the differences in apparent electrochemical potential experienced by ions in the sweat duct during secretion indicates that Na+ is held out of the lumen of both groups of ducts against a large but similar gradient, but that Cl- is held in the CF duct against a much larger gradient than in the normal duct. These results indicate that the mechanism for Na+ reabsorption is not inhibited in the CF duct, but that the decreased NaCl transport in the defective duct is due to an abnormally low permeability to Cl-. Analysis of the electrical potential as a function of the Cl- gradient in the sweat suggests that the normal and defective route of Cl- uptake may be transcellular.


1961 ◽  
Vol 200 (2) ◽  
pp. 309-312 ◽  
Author(s):  
C. S. Tidball

Characteristically water and chloride ion are absorbed from isotonic saline solutions placed in the in situ jejunal loop of the anesthetized dog. The direction of the water and chloride movement can be reversed by the administration of a cholinergic drug or by the addition of substituted phenols to the isotonic solution bathing the mucosal surface. During such secretion the movement of chloride occurs against a concentration gradient. The transmural electrical potential difference indicates that the lumen is negative with respect to the serosal surface during secretion; thus chloride is also moving against an electrical potential gradient. The calculated concentration of chloride in the fluid moving through the membrane during secretion is higher than the chloride concentration in extracellular fluid which indicates that solvent drag is not responsible for the chloride movement. Therefore active transport of chloride occurs during intestinal secretion.


1982 ◽  
Vol 97 (1) ◽  
pp. 197-216
Author(s):  
J. C. Cornell

1. Measurements of electrical potential difference (PD), short-circuit current (SCC) and unidirectional fluxes of sodium and chloride were made across portions of the intestine. Based on the results, the intestine can be divided into at least four physiologically distinct regions. 2. These four physiological regions, designated from anterior to posterior as R I-II, R III A, R III B and R IV, do not completely correspond to the four anatomically distinct regions of the intestine. 3. The PD (serosal side positive) in R I-II, R III A, R III B and R IV is 1.08, 12.4, 5.61 and 31.7 mV, respectively. 4. The SCC in these same regions is 9.9, 50.4, 49.7, and 16.4 micro A cm2, respectively. 5. When short-circuited, net sodium and net chloride fluxes in the above regions are −0.36 and −0.27, 1.46*** and −0.92*, 1.74*** and −0.06 and 1.01*** and 0.07 mumol cm-2 h-1, respectively. Positive fluxes indicate net mucosal to serosal movements and asterisks indicate significant net fluxes (* P less than 0.05, *** P less than 0.001). 6. There is good agreement between the SCC and net sodium transport in R III B. In the other regions of the intestine the ionic basis of the SCC has not been completely explained. 7. The properties of the intestine in vitro appear to make the intestine well suited for the task of conserving sodium, a function which the intestine performs in vivo.


1962 ◽  
Vol 203 (5) ◽  
pp. 873-880 ◽  
Author(s):  
James D. Finkelstein ◽  
David Schachter

The effects of hypophysectomy on active transport of calcium in vitro by everted gut sacs of rat duodenum are 1) an initial increase 4–5 days postoperatively and 2) a marked decrease 2–3 weeks postoperatively. The defect in transport results from reduction in the unidirectional transfers of Ca toward the serosa, and both steps in the transport (mucosal uptake and transfer to serosal surface) are impaired. Hypophysectomy also decreases iron transport (duodenal gut sacs), decreases l-proline transfer less strikingly (ileal gut sacs), increases d-galactose transport (jejunal gut sacs), and does not appear to influence either the electrical potential gradient from mucosa to serosa or the net flux of sodium. Treatment of hypophysectomized rats with a preparation of bovine growth hormone restores transfer mechanisms for calcium and iron. Ovine prolactin is also active in restoring the Ca mechanism, whereas other pituitary and nonpituitary hormones are not. Cortisone, l-thyroxin, and estradiol decrease Ca transport further in hypophysectomized rats. Absorption of Ca from loops of rat duodenum in vivo is also decreased 2 weeks after hypophysectomy and can be increased by prior treatment with bovine growth hormone.


1980 ◽  
Vol 239 (6) ◽  
pp. G463-G472 ◽  
Author(s):  
M. Donowitz ◽  
Y. H. Tai ◽  
N. Asarkof

The effect of serotonin on active electrolyte transport was evaluated in vitro in epithelial sheets of rabbit ileum, gallbladder, and colon under short-circuited conditions. Serotonin added to the serosal surface of rabbit ileum caused a dose-dependent short-lived increase in short-circuit current and a more prolonged equal effect on net Na and Cl fluxes. The latter consisted primarily of inhibition of mucosal-to-serosal fluxes of both Na and Cl. In addition serosal serotonin decreased ileal Na influx from the mucosal solution into the epithelium, suggesting an effect on Na absorption. Serotonin did not alter all aspects of ileal absorptive function and did not affect glucose-dependent Na absorption. Consistent with serotonin acting by inhibiting NaCl absorption in the ileum, serotonin induced equal inhibition of net Na and Cl absorption in rabbit gallbladder (which has a linked Na and Cl absorptive process) but had no effect on rabbit colon (which lacks a linked Na and Cl absorptive process). In addition, adenosine 3',5'-cyclic monophosphate and serotonin both appeared to alter the same ileal NaCl absorptive process, since following stimulation of ileal secretion with the maximum concentration of theophylline, addition of serotonin did not cause any further effects.


The epithelial cells of the rabbit ileum are about 40 µm long and have a diameter of roughly 5 µm. They are closely packed in a columnar fashion with their mucosal ends facing the lumen of the intestine and their serosal ends abutting the basement membrane and facing the underlying capillaries, lymphatics and connective tissue. The inner wall of the intestine is coated with a layer of mucopolysacharides, the mucus layer. When Krebs solution or similar solutions are placed in the lumen it is well known (e.g. the review by Edmonds 1970) that the solution is transported into the underlying tissues. During this transport the sodium activity in the gut lumen remains constant, the chloride activity decreases and the bicarbonate activity increases. However, the relationship of the intra- to the extracellular environment of each individual cell during this transport is only little understood. In recent years the methods applied in the study of the state of the cells during this transport have mostly been of a type that requires preparation of the tissue in vitro , e.g. usage of flamephotometry and Ussing-chambers. In case of the intestine of warm-blooded animals such a choice of experimental conditions is unfortunate for several reasons: ( a ) The transport is no longer into the blood or lymphatic drainage, ( b ) the epithelial cells have to be oxygenated from their luminal ends which in vivo are normally at a very low oxygen concentration (Crompton, Silver & Shrimpton 1965) and ( c ) in some experiments the physiological parameters of the tissue change during the experiment (e.g. Powell, Binder & Curran 1973). However, the use of microelectrodes allows an in vivo approach since the tissue can be left in its natural environment during the measurements. Furthermore liquid ion exchanges and ion-sensitive glasses developed over the past few years have led to the construction of microelectrodes selective to various ions (Hinke 1959; Thomas 1970; Walker 1971), so that the state of cells in terms of intra- and extracellular electrical potential and ion activities can be determined. Thus intracellular sodium and potassium has been recorded in the epithelial cells of the bullfrog small intestine in vitro (Lee & Armstrong 1972). The purpose of this work was first to construct an in vivo model in which the epithelial cell layer of the rabbit ileum could be studied by microelectrodes and secondly to determine the intra and extracellular electrical potential and ion activities in these cells when the lumen of the intestine was filled with various salt solutions.


1974 ◽  
Vol 64 (3) ◽  
pp. 274-292 ◽  
Author(s):  
Jehan-F. Desjeux ◽  
Y.-H. Tai ◽  
Peter F. Curran

Sodium flux from serosa to mucosa, JsmNa in rabbit ileum in vitro has been studied as a function of applied electrical potential at equal sodium concentrations in the bathing solutions. The results indicate that JsmNa involves two pathways, a diffusional flux through a paracellular shunt pathway and a flux that is independent of applied potential and presumably involves a transcellular pathway. The latter pathway comprises approximately 25 % of JsmNa in Ringer's solution containing 10 mM glucose and 25 mM bicarbonate. It is stimulated significantly by theophylline unaffected by removal of glucose or addition of ouabain but is reduced to negligible values by anoxia, dinitrophenol, and replacement of all chloride and bicarbonate by isethionate. Thus this component of JsmNa has a number of characteristics consistent with involvement in a specific secretory process mediating an electrically neutral secretory transport of sodium plus anion from serosa to mucosa. In addition to stimulating this process, theophylline significantly reduced the permeability of the paracellular shunt pathway to sodium.


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