Sodium and Water Transport Across the Jejunum of Fasted Rats

1973 ◽  
Vol 51 (6) ◽  
pp. 405-409 ◽  
Author(s):  
Ivan T. Beck ◽  
P. K. Dinda
Keyword(s):  
Sodium Transport ◽  
Fluid Transport ◽  
Electrical Potential ◽  
Electrical Potential Difference ◽  
Serosal Side ◽  
Concomitant Increase ◽  
Net Flux ◽  
Unidirectional Fluxes ◽  
Mucosal Side ◽  
Fasted Rats

The effect of 72 h fasting on the transmural electrical potential difference (P.D.), the unidirectional fluxes, and the net flux of sodium and the net transport of fluid across the jejunum of rats was investigated. Everted jejunal segments were incubated in 12 ml of Krebs–Ringer bicarbonate solution containing 5.55 mM glucose on either side for 1 h at 37 °C. Seventy-two hours fasting caused a 63% increase in the transmural P.D., a 60% increase in the flux of Na from the mucosal to the serosal side, and a 48% increase in the flux of Na from the serosal to the mucosal side. The net mucosal to serosal Na flux increased by 97%. There was also a 41% increase in fluid transport across the intestine of fasted rats. The concomitant increase in sodium and fluid transport and in transmural P.D. is consistent with the current hypotheses of fluid and sodium transport.

Sodium transport and the cellular sodium transport pool of colonic epithelium: effects of sodium loading, aldosterone and lithium

1987 ◽  
Vol 112 (2) ◽  
pp. 247-252 ◽  
Author(s):  
C. J. Edmonds ◽  
J. Mackenzie
Keyword(s):  
Epithelial Cells ◽  
Sodium Transport ◽  
Time Course ◽  
Electrical Potential ◽  
Electrical Potential Difference ◽  
Active Sodium ◽  
Prolonged Infusion ◽  
Sodium Loading ◽  
Sodium Flux

ABSTRACT The cellular sodium transport pool and sodium transepithelial fluxes were investigated in vivo in rat distal colon in relation to sodium loading by intravenous infusion (3·5 h), and to short (4 h) and prolonged (72 h) i.v. administration of aldosterone. Considerable natriuresis and increase in body sodium content were produced by the sodium load but there was no significant effect on the transcellular sodium flux (active absorption from lumen to plasma) or on the sodium transport pool. Both short and prolonged aldosteronism produced similar increases in the transport pool and in the transcellular sodium flux, but the transepithelial electrical potential difference (p.d.) was significantly greater in rats given the prolonged infusion. Addition of amiloride to the solution in the lumen of the colon almost completely abolished the p.d., the transport pool and the transcellular sodium flux of the rats receiving prolonged infusion, but had much less effect in those given the short infusion. The time-course of recovery of p.d. following prolonged aldosteronism was similar to that described for the turnover rate of rat colonic epithelial cells. Lithium within the lumen had no significant effect in untreated rats but after prolonged aldosterone infusion lithium reduced the p.d. and the transcellular sodium flux although the transport pool was not reduced. These findings are consistent with the hypothesis that aldosteronism renders the apical membranes of the epithelial cells permeable to lithium and that intracellular accumulation of lithium depresses active sodium transfer. The observations are interpreted in terms of an epithelial model in which aldosterone induces amiloride-sensitive pathways (diffusion channels permeable to sodium and lithium) in the apical membrane which totally replace the amiloride-insensitive pathways when aldosteronism is prolonged; the resulting expansion of the sodium transport pool is the stimulus for increased active sodium transport across the basolateral membranes. J. Endocr. (1987) 112, 247–252

An Investigation of the Role of Possible Neural Mechanisms in Cholera Toxin-Induced Secretion in Rabbit Ileal Mucosa in Vitro

1989 ◽  
Vol 77 (2) ◽  
pp. 161-166 ◽  
Author(s):  
K. J. Moriarty ◽  
N. B. Higgs ◽  
M. Woodford ◽  
L. A. Turnberg
Keyword(s):  
Cholera Toxin ◽  
Fluid Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Rabbit Ileum ◽  
Ileal Mucosa

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.

scholarly journals Energetics of Sodium Transport in Frog Skin

1972 ◽  
Vol 59 (1) ◽  
pp. 77-91 ◽  
Author(s):  
F. L. Vieira ◽  
S. R. Caplan ◽  
A. Essig
Keyword(s):  
Free Energy ◽  
Oxygen Consumption ◽  
Sodium Transport ◽  
Frog Skin ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Rate Of Oxygen Consumption ◽  
Phenomenological Coefficients

Studies were made of the dependence of the rate of oxygen consumption, Jr, on the electrical potential difference, Δψ, across the frog skin. After the abolition of sodium transport by ouabain the basal oxygen consumption was independent of Δψ. In fresh skins Jr was a linear function of Δψ over a range of at least ±70 mv. Treatment with aldosterone stimulated the short-circuit current, Io, and the associated rate of oxygen consumption, Jro, and increased their stability; linearity was then demonstrable over a range of ±160 mv. Brief perturbations of Δψ (±30–200 mv) did not alter subsequent values of Io. Perturbations for 10 min or more produced a "memory" effect both with and without aldosterone: accelerating sodium transport by negative clamping lowered the subsequent value of Io; positive clamping induced the opposite effect. Changes in Jro were more readily detectable in the presence of aldosterone; these were in the same direction as the changes in Io. The linearity of Jr in Δψ indicates the validity of analysis in terms of linear nonequilibrium thermodynamics—brief perturbations of Δψ appear to produce no significant effect on either the phenomenological coefficients or the free energy of the metabolic driving reaction. Hence it is possible to evaluate this free energy.

Steroid metabolism determines mineralocorticoid specificity in the toad bladder

1989 ◽  
Vol 257 (4) ◽  
pp. F690-F695 ◽  
Author(s):  
H. P. Gaeggeler ◽  
C. R. Edwards ◽  
B. C. Rossier
Keyword(s):  
Sodium Transport ◽  
Potent Inhibitor ◽  
Toad Bladder ◽  
Base Line ◽  
Mineralocorticoid Receptors ◽  
Serosal Side ◽  
Maximal Increase ◽  
Inactive Metabolite ◽  
Mucosal Side

Edwards et al. (C. R. W. Edwards, P. M. Stewart, D. Burt, L. Brett, M. A. McIntyre, W. S. Sutanto, E. R. de Kloet, and C. Monder, Lancet 2: 986-989, 1988) proposed that 11 beta-hydroxysteroid-dehydrogenase (11 beta-OHSD) plays a key role in the kidney by converting glucocorticoids (cortisol or corticosterone), which display a high affinity for type 1 mineralocorticoid receptors, into their inactive metabolites (cortisone or 11-dehydroxy-corticosterone), thus preventing their illicit occupation of the receptor in the target cell for aldosterone. We have tested this hypothesis in the urinary bladder of Bufo marinus by measuring the sodium transport responses to aldosterone and corticosterone. Aldosterone (10 nM) on the serosal side elicited a quarter of the maximal increase in sodium transport. At the same concentration, corticosterone (10 nM, serosal side) was ineffective. Adding corticosterone (10 nM) on the mucosal side elicited a response equivalent to that of aldosterone, suggesting that corticosterone was inactivated in the serosal or underlying tissue of the toad bladder. Carbenoxolone (10 microM, serosal side), a potent inhibitor of 11 beta-OHSD, did not modify the base-line sodium transport. However, in the presence of carbenoxolone (10 microM, serosal side, 2 h pretreatment) corticosterone (10 nM, serosal side) became as potent as aldosterone in eliciting the mineralocorticoid response. Our data are consistent with the idea that corticosterone is converted into an inactive metabolite in the mucosal and/or submucosal tissue of the toad bladder. These studies are consistent with our concept that 11 beta-OHSD is crucial in protecting the nonspecific mineralocorticoid receptor from glucocorticoid.

Intravenous indomethacin and aspirin reduce basal gastric mucosal blood flow in dogs

1980 ◽  
Vol 238 (2) ◽  
pp. G131-G134 ◽  
Author(s):  
G. L. Kauffman ◽  
D. Aures ◽  
M. I. Grossman
Keyword(s):  
Blood Flow ◽  
Electrical Potential ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Prostaglandin Synthesis ◽  
Electrical Potential Difference ◽  
Heidenhain Pouch ◽  
Endogenous Prostaglandin ◽  
Net Flux ◽  
Change In Mean

The effect of two known inhibitors of prostaglandin synthesis, indomethacin and aspirin, on blood flow was studied in six Heidenhain pouch and three antral pouch dogs. The unstimulated gastric mucosa was bathed with 0.15 M HCl and clearance of [14C]-aminopyrine was used as an index of changes in mucosal blood flow. [14C]aminopyrine clearance was measured during three 15-min predrug periods and five 15 min-postdrug periods. Either indomethacin (10 mg . kg-1), aspirin (100 mg . kg-1), or 0.15 M NaCl were given intravenously as a bolus. Indomethacin reduced mucosal blood flow in the Heidenhain pouch 52% (P less than 0.05) and in the antral pouch 52% (P less than 0.05). Aspirin reduced Heidenhain pouch mucosal blood flow 31% (P less than 0.05). Indomethacin caused no significant change in electrical potential difference or in net flux of H+ or Na+ in Heidenhain pouches. Indomethacin (10 mg . kg-1 iv) produced no change in mean arterial pressure. We conclude that indomethacin and aspirin reduce unstimulated gastric mucosal blood flow, suggesting that endogenous prostaglandin may contribute to its maintenance.

Transport of electrolytes and water across wall of rabbit gall bladder

1963 ◽  
Vol 205 (3) ◽  
pp. 427-438 ◽  
Author(s):  
Henry O. Wheeler
Keyword(s):  
Solute Transport ◽  
Active Transport ◽  
Water Movement ◽  
Water Flux ◽  
Electrical Potential ◽  
Flux Ratio ◽  
Coupling Mechanism ◽  
Electrical Potential Difference ◽  
Net Flux

Gall bladders of rabbits were studied in vitro in an apparatus which permitted measurement of electrical potential difference, net flux of water, and changes in electrolyte concentrations in mucosal and serosal fluid. Net water flux (mucosa to serosa) was directly proportional to net solute transport (measured as sodium flux) and the transported solution was slightly hypertonic. When mannitol was added to the mucosal fluid, water movement occurred against osmotic gradients often exceeding 80 mosmol/kg. Electrical potential differences were small, but the lumen was invariably positive. Flux ratio determinations indicated active transport of both chloride and sodium but not potassium. When isethionate was substituted for chloride, active bicarbonate absorption was also evident. Anion and cation transport were not independent and no transport occurred when choline was substituted for sodium. The evidence suggests coupled active transport of sodium and the major anions. Water movement is dependent upon active solute transport by means of an undetermined coupling mechanism.

Fluid transport across the canine tracheal epithelium

1980 ◽  
Vol 49 (5) ◽  
pp. 905-909 ◽  
Author(s):  
M. J. Welsh ◽  
J. H. Widdicombe ◽  
J. A. Nadel
Keyword(s):  
Fluid Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Fluid Secretion ◽  
Volume Flow ◽  
Tracheal Epithelium ◽  
Base Line ◽  
Electrical Method ◽  
Cl Secretion ◽  
Net Flux

We measured the rate of fluid movement across the tracheal epithelium of the dog by an electrical method, modified from that originally described by Wiedner (Rev. Sci. Instrum. 47: 775-6, 1976). The base-line volume flow (Jv) from the submucosa to the mucosa was 44 +/- 23 nl.min-1.cm-2 (mean +/- SE; n = 6). In only three of the tissues was the resting Jv significantly greater than zero. Stimulation with 2 X 10(-3) M aminophylline (a drug that we have shown stimulates Cl secretion under short-circuit conditions) increased Jv in all tissues to a mean of 137 +/- 29 nl.min-1.cm-2 (P < 0.001). We also measured the unidirectional fluxes of Cl with the tissue at its spontaneous electrical potential. During the base-line period, the net flux of Cl was not significantly different from zero. During stimulation with aminophylline, Cl secretion increased to a mean of 1.44 +/- 0.50 microneq.cm-2.h-1. Comparison of the stimulated values of Jv and net Cl secretion suggests that fluid secretion by the trachea is isotonic during stimulation with aminophylline.

scholarly journals Partitioning of Acid-Base Regulation Between Renal and Extrarenal Sites in the Adult, Terrestrial Stage of the Salamander Ambystoma Tigrinum During Respiratory Acidosis

1991 ◽  
Vol 157 (1) ◽  
pp. 47-62 ◽  
Author(s):  
DANIEL F. STIFFLER
Keyword(s):  
Renal Involvement ◽  
Electrical Potential ◽  
Respiratory Acidosis ◽  
Ambystoma Tigrinum ◽  
Electrical Potential Difference ◽  
Acid Base ◽  
Total Ammonia ◽  
Unidirectional Fluxes ◽  
Na Uptake ◽  
Partial Compensation

Adult Ambystoma tigrinum were cannulated non-occlusively in the truncus arteriosus and subjected to 24 h of hypercapnia in 3% CO2. Adults showed the typical compensatory pattern, shared by larvae and many other amphibians, of partial compensation (44%) for the induced respiratory acidosis. Adults whose urinary bladders were ligated to allow the urine to bypass the bladder compensated as well as shams, indicating that the urinary bladder of this species is not necessary for compensation. Radioisotopic measurements of net and unidirectional fluxes of Na+ or Cl− in whole animals showed no effects of hypercapnia. Partitioning of acid-base responses showed that 75–80 % of the regulation takes place across the skin. The rest is accomplished by the kidneys. This did not change during hypercapnia and there was no evidence of renal involvement in the compensation. Total ammonia (NH3+NH4+) comprised only about one-sixth of the total cutaneous acid excretion. The charge associated with the cutaneous excretion of H+ equivalents was balanced by both Na+ uptake and Cl− loss. In contrast to larvae, whose cutaneous electrical potential difference (PD) increases during hypercapnia, adults decrease their PD. This could mean that acidosis stimulates an electrogenic H+ secretion and/sor that cutaneous Na+ and Cl− permeabilities change. Both possibilities are consistent with the data.

ALDOSTERONE, SODIUM DEPLETION AND HYPOTHYROIDISM ON THE ATPASE ACTIVITY OF RAT COLONIC EPITHELIUM

1974 ◽  
Vol 62 (3) ◽  
pp. 489-496 ◽  
Author(s):  
B. D. THOMPSON ◽  
C. J. EDMONDS
Keyword(s):  
Atpase Activity ◽  
Sodium Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Rat Colon ◽  
Electrical Potential Difference ◽  
Sodium Depletion ◽  
Active Sodium ◽  
Active Sodium Transport ◽  
Sodium Dependent

SUMMARY Transmucosal electrical potential difference and short-circuit current of an in-vitro preparation of mucosal epithelium of rat colon were almost abolished and active sodium transport ceased when ouabain (1 mmol/l) was present on the serosal side of the epithelium. A considerable fraction of the total ATPase activity in the mucosa was sodium dependent and concentrations of ouabain of 0·5 mmol/l or more completely eliminated the activity of this fraction. Adenosine triphosphatase activities in mucosa taken from normal, hypothyroid, aldosterone-treated and sodium-depleted rats were compared. The activity of the ouabain-sensitive, sodium-dependent fraction was similar in all groups except for the hypothyroid rats in which it was considerably reduced. There was no evidence from the present study that the increased active sodium transport by colonic mucosa, associated with aldosterone action or sodium depletion, depended upon a change in ATPase activity. In hypothyroidism, reduction of ouabain-sensitive ATPase activity may be responsible for the observed impairment of the sodium transport mechanism.

Sign in / Sign up

Export Citation Format

Share Document