scholarly journals A mathematical model of the inner medullary collecting duct of the rat: pathways for Na and K transport

1998 ◽  
Vol 274 (5) ◽  
pp. F841-F855 ◽  
Author(s):  
Alan M. Weinstein
Keyword(s):  
Mathematical Model ◽  
Cell Membrane ◽  
Collecting Duct ◽  
High Rate ◽  
Inner Medullary Collecting Duct ◽  
Luminal Membrane ◽  
Medullary Collecting Duct ◽  
Model Features ◽  
Novel Model ◽  
Nacl Cotransport

A mathematical model of the inner medullary collecting duct (IMCD) of the rat has been developed representing Na+, K+, Cl−,[Formula: see text] CO2, H2CO3, phosphate, ammonia, and urea. Novel model features include: finite rates of hydration of CO2, a kinetic representation of the H-K-ATPase within the luminal cell membrane, cellular osmolytes that are regulated in defense of cell volume, and the repeated coalescing of IMCD tubule segments to yield the ducts of Bellini. Model transport is such that when entering Na+ is 4% of filtered Na+, approximately 75% of this load is reabsorbed. This requirement renders the area-specific transport rate for Na+ comparable to that for proximal tubule. With respect to the luminal membrane, there is experimental evidence for both NaCl cotransport and an Na+ channel in parallel. The experimental constraints that transepithelial potential difference is small and that the fractional apical resistance is greater than 85% mandate that more than 75% of luminal Na+ entry be electrically silent. When Na+delivery is limited, an NaCl cotransporter can be effective at reducing luminal Na+ concentration to the observed low urinary values. Given the rate of transcellular Na+ reabsorption, there is necessarily a high rate of peritubular K+recycling; also, given the lower bound on luminal membrane Cl− reabsorption, substantial peritubular Cl− flux must be present. Thus, if realistic limits on cell membrane electrical resistance are observed, then this model predicts a requirement for peritubular electroneutral KCl exit.

scholarly journals A mathematical model of the inner medullary collecting duct of the rat: acid/base transport

1998 ◽  
Vol 274 (5) ◽  
pp. F856-F867 ◽  
Author(s):  
Alan M. Weinstein
Keyword(s):  
Mathematical Model ◽  
Acid Secretion ◽  
Collecting Duct ◽  
Model Calculations ◽  
Principal Mode ◽  
Inner Medullary Collecting Duct ◽  
Tubule Lumen ◽  
Nephron Segment ◽  
The Face ◽  
Medullary Collecting Duct

A mathematical model of the inner medullary collecting duct (IMCD) of the rat has been developed that is suitable for simulating luminal buffer titration and ammonia secretion by this nephron segment. Luminal proton secretion has been assigned to an H-K-ATPase, which has been represented by adapting the kinetic model of the gastric enzyme by Brzezinski et al. (P. Brzezinski, B. G. Malmstrom, P. Lorentzon, and B. Wallmark. Biochim. Biophys. Acta 942: 215–219, 1988). In shifting to a 2 H+:1 ATP stoichiometry, the model enzyme can acidify the tubule lumen ∼3 pH units below that of the cytosol, when luminal K+ is in abundance. Peritubular base exit is a combination of ammonia recycling and[Formula: see text] flux (either via[Formula: see text] exchange or via a Cl− channel). Ammonia recycling involves[Formula: see text] uptake on the Na-K-ATPase followed by diffusive NH3 exit [S. M. Wall. Am. J. Physiol. 270 ( Renal Physiol. 39): F432–F439, 1996]; model calculations suggest that this is the principal mode of base exit. By virtue of this mechanism, the model also suggests that realistic elevations in peritubular K+ concentration will compromise IMCD acid secretion. Although ammonia recycling is insensitive to carbonic anhydrase (CA) inhibition, the base exit linked to [Formula: see text] flux provides a CA-sensitive component to acid secretion. In model simulations, it is observed that increased luminal NaCl entry increases ammonia cycling but decreases peritubular [Formula: see text]exchange (due to increased cell Cl−). This parallel system of peritubular base exit stabilizes acid secretion in the face of variable Na+ reabsorption.

scholarly journals Intracellular pH regulation in freshly isolated suspensions of rabbit inner medullary collecting duct cells: role of Na+:H+ antiporter and H(+)-ATPase.

1990 ◽  
Vol 1 (6) ◽  
pp. 890-901
Author(s):  
D Kikeri ◽  
M L Zeidel
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Intracellular Ph ◽  
Recovery Rate ◽  
Collecting Duct ◽  
Atp Depletion ◽  
Cell Membrane Potential ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
In Cells

To define proton transport mechanisms involved in the regulation of intracellular pH (pHi) in cells of the inner medullary collecting duct (IMCD), pHi and cell membrane potential were estimated by using the fluorescent dyes 2,7-biscarboxyethyl-5(6)-carboxyfluorescein and 3,3'-dipropylthiadicarbocyanine iodide, respectively, in suspensions of freshly isolated rabbit IMCD cells. The resting pHi of IMCD cells in nonbicarbonate Ringer's solution (pH 7.4) was 7.21 +/- 0.03 (mean +/- SE). When cells were acidified by ammonium withdrawal, the initial pHi recovery rate was 0.33 +/- 0.02 pH unit/min; replacement of extracellular Na+ (130 mM) with N-methyl-D-glucamine+ reduced the pHi recovery rate to 0.08 +/- 0.02 pH unit/min, while addition of 0.1 mM amiloride in the presence of extracellular Na+ reduced the rate of pHi recovery to 0.02 +/- 0.02 pH unit/min. Similar results were obtained in cells acid loaded with HCl. Cells recovering from acidification exhibited 22Na+ uptake rates threefold higher than did nonacidified cells. The rate of Na(+)-dependent pHi recovery was independent of the cell membrane potential. In the absence of extracellular Na+, depolarizing cell membrane potential in a stepwise manner by increasing extracellular K+ concentrations from 1 to 130 mM resulted in graded increments in the rate of pHi recovery. In the presence of 130 mM K+, the pHi recovery rate in acidified cells was dependent on cellular ATP levels, sensitive to 1 mM N-ethylmaleimide, and insensitive to 0.01 mM oligomycin in the presence of glucose (control, 0.24 +/- 0.01; ATP-depleted, 0.13 +/- 0.02; addition of N-ethylmaleimide, 0.16 +/- 0.01; addition of oligomycin, 0.27 +/- 0.02 pH unit/min). ATP depletion markedly inhibited H+ extrusion from IMCD cells measured by using a pH stat. These results provide direct evidence in freshly isolated IMCD cells that both a Na+:H+ antiporter and a rheogenic H(+)-ATPase participate in pHi regulation.

Calcium transport across rat inner medullary collecting duct perfused in vitro

1989 ◽  
Vol 257 (5) ◽  
pp. F738-F745 ◽  
Author(s):  
A. J. Magaldi ◽  
A. A. van Baak ◽  
A. S. Rocha
Keyword(s):  
Collecting Duct ◽  
Diffusion Mechanism ◽  
Direct Determination ◽  
Na Transport ◽  
Inner Medullary Collecting Duct ◽  
Luminal Membrane ◽  
Perfusion Solution ◽  
Medullary Collecting Duct ◽  
The Difference

Ca2+ transport by the inner medullary collecting duct (IMCD) of normal rats was studied using the "in vitro" microperfusion technique. Net (Jnet), lumen-to-bath (Jl----b), and bath-to-lumen (Jb----l) fluxes of Ca2+ were measured in the absence of net water absorption using 45Ca as a tracer. In the absence of an electrochemical gradient, an important net absorption of Ca2+ (11.1 +/- 1.6 pmol.cm-2.s-1), similar to the difference between the Jl----b and Jb----l, was observed by direct determination at low (5-6 nl/min) and high (12-17 nl/min) perfusion rates. The Jl----b of Ca2+ was reduced by the addition to the bath fluid of ouabain (10(-3) M) and verapamil (10(-4) M), by the presence of amiloride (10(-5) and 10(-3) M) and verapamil (10(-4) M) in the luminal fluid, or by perfusion with a Na+-free solution. Neither the presence of verapamil (10(-4) M) and ouabain (10(-3) M) in the bath nor the withdrawal of Na+ from bath and perfusion solution was able to modify the Jb----l of Ca2+. Incrementing Ca2+ bath concentration increased proportionally the Jb----l of Ca2+. Therefore Ca2+ outflux is in part dependent on Na+-K+-adenosinetriphosphatase luminal membrane Na+ transport and in part inhibited by verapamil. However, Ca2+ influx is independent of Na+ transport, is not blocked by verapamil, but is increased by Ca2+ transtubular gradient, indicating the presence of a passive diffusion mechanism.

Water permeability of apical and basolateral cell membranes of rat inner medullary collecting duct

1990 ◽  
Vol 259 (6) ◽  
pp. F986-F999 ◽  
Author(s):  
B. Flamion ◽  
K. R. Spring
Keyword(s):  
Water Flow ◽  
Water Permeability ◽  
Cell Membranes ◽  
Apical Membrane ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Volume Regulatory Decrease ◽  
Water Permeation ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

To quantify the pathways for water permeation through the kidney medulla, knowledge of the water permeability (Posmol) of individual cell membranes in inner medullary collecting duct (IMCD) is required. Therefore IMCD segments from the inner two thirds of inner medulla of Sprague-Dawley rats were perfused in vitro using a setup devised for rapid bath and luminal fluid exchanges (half time, t1/2, of 55 and 41 ms). Differential interference contrast microscopy, coupled to video recording, was used to measure volume and approximate surface areas of single cells. Volume and volume-to-surface area ratio of IMCD cells were strongly correlated with their position along the inner medullary axis. Transmembrane water flow (Jv) was measured in response to a variety of osmotic gradients (delta II) presented on either basolateral or luminal side of the cells. The linear relation between Jv and delta II yielded the cell membrane Posmol, which was then corrected for membrane infoldings. Basolateral membrane Posmol was 126 +/- 3 microns/s. Apical membrane Posmol rose from a basal value of 26 +/- 3 microns/s to 99 +/- 5 microns/s in presence of antidiuretic hormone (ADH). Because of amplification of basolateral membrane, the ADH-stimulated apical membrane remained rate-limiting for transcellular osmotic water flow, and the IMCD cell did not swell significantly. Calculated transcellular Posmol, expressed in terms of smooth luminal surface, was 64 microns/s without ADH and 207 microns/s with ADH. IMCD cells in anisosmotic media displayed almost complete volume regulatory decrease but only partial volume regulatory increase.

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