scholarly journals Models for coupling of salt and water transport; Proximal tubular reabsorption in Necturus kidney.

1975 ◽  
Vol 66 (6) ◽  
pp. 671-733 ◽  
Author(s):  
H Sackin ◽  
E L Boulpaep
Keyword(s):  
Water Transport ◽  
Epithelial Transport ◽  
Driving Forces ◽  
Water Fluxes ◽  
Transport Parameters ◽  
Na Transport ◽  
Continuous Version ◽  
Leaky Epithelia ◽  
Proximal Tubular ◽  
Proximal Tubular Reabsorption

Models for coupling of salt and water transport are developed with two important assumptions appropriate for leaky epithelia. (a) The tight junction is permeable to both sale and water. (b) Active Na transport into the lateral speces is assumed to occur uniformly along the length of the channel. The proposed models deal specifically with the intraepithelial mechanism of proximal tubular resbsorption in the Necturus kidney although they have implications for epithelial transport in the gallbladder and small intestine as well. The first model (continuous version) is similar to the standing gradient model devised by Diamond and Bossert but used different boundary conditions. In contrast to Diamond and Bossert's model, the predicted concentration profiles are relatively flat with no sizable gradients along the interspace. The second model (compartment version) expands Curran's model of epithelial salt and water transport by including additional compartments and considering both electrical and chemical driving forces for individual Na and Cl ions as well as hydraulic and osmotic driving forces for water. In both models, ion and water fluxes are investigated as a function of the transport parameters. The behavior of the models is consistent with previously suggested mechanisms for the control of net transport, particularly during saline diuresis. Under all conditions the predicted ratio of net solute to solvent flux, or emergent concentration, deviates from exact isotonicity (except when the basement membrane has an appreciable salt reflection coefficient). However, the degree of hypertonicity may be small enough to be experimentally indistinguishable from isotonic transport.

Epithelial transport parameters: an analysis of experimental strategies

1983 ◽  
Vol 218 (1212) ◽  
pp. 309-329 ◽  
Keyword(s):  
Experimental Data ◽  
Epithelial Transport ◽  
Flux Ratio ◽  
Model Parameters ◽  
Acta Physiol ◽  
Transport Parameters ◽  
Na Transport ◽  
Experimental Conditions ◽  
System Parameters ◽  
Experimental Strategies

A set of experiments was simulated on a computer version of the Koefoed-Johnsen & Ussing model for high-resistance epithelia. The results obtained were analysed according to procedures commonly applied to the analyses of experimental data and interpreted in terms of the model parameters. Although the computer model encodes a stoichiometry of 3:2 for Na-K exchange through the Na pump, the simulation of published experimental procedures yields different figures in almost every case. We show that E Na as originally defined by Ussing & Zerahn ( Acta physiol. scand . 23, 110-127 (1951)) and as obtained from flux-ratio experiments has different values under different experimental conditions with unchanged system parameters and that it is distinct from E Na measured by other methods. We also show that unless the pump is saturated with internal Na an increase in the rate of pumping cannot cause a substantial increase in the rate of transepithelial Na transport.

Can causality be determined from proximal tubular reabsorption and peritubular physical factors?

1986 ◽  
Vol 250 (1) ◽  
pp. F169-F175 ◽  
Author(s):  
B. J. Tucker ◽  
C. A. Mundy ◽  
R. C. Blantz
Keyword(s):  
Steady State ◽  
Epithelial Transport ◽  
Capillary Flow ◽  
Tubular Reabsorption ◽  
Physical Factors ◽  
Peritubular Capillary ◽  
Fluid Uptake ◽  
Before And After ◽  
Proximal Tubular ◽  
Proximal Tubular Reabsorption

Many studies in the literature have drawn conclusions regarding the mechanism of change in absolute proximal tubular reabsorption (APR) based on steady-state measurements of proximal reabsorptive rates and the peritubular capillary. The proximal reabsorptive rate, APR, is the product of the effective reabsorptive pressure (ERP) and the peritubular capillary reabsorptive coefficient (LpAR) (APR = ERP . LpAR). The ERP is defined by the net hydrostatic and oncotic pressure gradient acting across the capillary wall from interstitium to peritubular capillary flow. The relationship APR = ERP . LpAR is predefined, and steady-state measurements do not permit determination of causality because primary changes in any variable obligate a proportional change in a second variable. As an example of the difficulties in interpretation of this type of analysis, we have examined the APR and factors contributing to ERP and LpAR before and after the administration of benzolamide, a carbonic anhydrase inhibitor, to saline-expanded Munich-Wistar rats. Alterations in peritubular capillary fluid uptake cannot always be interpreted as casual mechanisms for changes in absolute fluid reabsorption but may result from primary alterations in epithelial transport.

Mineral Excretion by Low Birth Weight Infants

1990 ◽  
Vol 12 (4) ◽  
pp. 101-127
Keyword(s):  
Birth Weight ◽  
Low Birth Weight ◽  
Very Low Birth Weight ◽  
Term Infant ◽  
Sodium Reabsorption ◽  
Vlbw Infant ◽  
Low Birth Weight Infants ◽  
Fourfold Increase ◽  
Proximal Tubular ◽  
Proximal Tubular Reabsorption

The preterm, low or very low birth weight (VLBW) infant has several inadequate homeostatic mechanisms, among which renal immaturity is prominent. Maximal renal concentrating ability in the VLBW infant is often less than twice the osmolality of plasma, compared to a fourfold increase in the mature infant. Equally important is the VLBW infant's limited proximal tubular reabsorption of sodium. The mature infant's response to sodium restriction results in over 99.5% of filtered sodium being reabsorbed; in the case of the VLBW infant, sodium reabsorption may be only 97% to 98% from days 4 through 14 of life. As a result of these two important limits, the VLBW infant has a higher water requirement than the full-term infant.

Dopamine inhibits AVP-dependent Na+ transport and water permeability in rat CCD via a D4-like receptor

1996 ◽  
Vol 271 (2) ◽  
pp. F391-F400 ◽  
Author(s):  
D. Sun ◽  
J. A. Schafer
Keyword(s):  
Water Transport ◽  
Water Permeability ◽  
Sch 23390 ◽  
Na Transport ◽  
D2 Agonist ◽  
Osmotic Water ◽  
D1 Agonists ◽  
Transepithelial Voltage ◽  
Specific Antagonist ◽  
Type Receptor

We studied the receptor responsible for dopamine action in isolated perfused cortical collecting ducts (CCD) from rats treated with deoxy-corticosterone. (Critical experiments were repeated in CCD from untreated rats with the same results.) At doses > or = 1 microM, dopamine inhibited arginine vasopressin (AVP)-dependent Na+ and water transport (measured by the unidirectional lumen-to-bath 22Na+ flux and the transepithelial voltage) and osmotic water permeability (Pf). The effects of dopamine were not reversed by the dopamine-1 (D1) antagonist SCH-23390, and no inhibition was produced by the D1 agonists fenoldopam or SKF-81247. When Na+ transport and Pf were stimulated with 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate plus 3-isobutyl-1-methylxanthine, dopamine did not inhibit, suggesting a "D2-type" receptor. However, the D2 agonist quinpirole had no effect on the AVP-dependent transepithelial voltage (VT), and the D2 and D3 antagonists domperidone and pimozide did not reverse dopamine inhibition of VT. The only agent tested that reversed the effects of dopamine was the D4-specific antagonist clozapine. We conclude that dopamine inhibition of salt and water transport in the CCD is mediated by a D4-like receptor.

Dissociation of proximal tubular glucose and Na+ reabsorption by amphotericin B

1979 ◽  
Vol 236 (4) ◽  
pp. F392-F397
Author(s):  
P. S. Aronson ◽  
J. P. Hayslett ◽  
M. Kashgarian
Keyword(s):  
Proximal Tubule ◽  
Glucose Uptake ◽  
Amphotericin B ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Na Transport ◽  
Glucose Reabsorption ◽  
Tubular Lumen ◽  
Proximal Tubular ◽  
Necturus Proximal Tubule

The effect of amphotericin B on glucose and Na+ transport was studied in the Necturus proximal tubule and in microvillus membrane vesicles isolated from the rabbit renal cortex. In the Necturus experiments, the rate constants for disappearance of radiolabeled glucose (kG) and mannitol (kM) from the tubular lumen were determined by stop-flow microperfusion. Saturability and Na+-dependence of glucose reabsorption was confirmed, since kG was reduced by raising intratubular glucose from 1 to 5 mM or by replacing intratubular Na+ with choline. Neither maneuver affected kM. Intratubular amphotericin B (10 microgram/ml), previously shown to stimulate active Na+ reabsorption in the Necturus proximal tubule, inhibited kG with no effect on kM. In the membrane vesicle preparation, amphotericin inhibited the uphill glucose uptake which results from imposing a NaCl gradient from outside to inside, but had no effect on glucose uptake in either the absence of Na+ or in the presence of Na+ when there was no Na+ gradient. Amphotericin B stimulated the uptake of Na+ by the vesicles. The observed dissociation of glucose and Na+ transport by amphotericin B is consistent with the concept that proximal tubular glucose reabsorption is energized by the luminal membrane Na+ gradient and is not directly linked to active Na+ transport per se.

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