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Mechanism of Fluid Transport by Epithelia

Kenneth R. Spring

10.1002/cphy.cp060405

Source: Supplement 19: Handbook of Physiology, The Gastrointestinal System, Intestinal Absorption and Secretion

Originally published: 1991

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Structure‐Function Correlations
2 Isosmotic Fluid Transport: Approximation or Reality
3 Movement of Water Through Membranes and Tight Junctions
4 Models of Epithelial Fluid Transport
5 Water Permeability of Epithelial Tissues
5.1 Cell Membrane Water Permeability
5.2 Route of Transepithelial Fluid Flow
6 Osmotic Driving Force Required for Transepithelial Flow
6.1 Transcellular Osmosis
6.2 Mechanism of Fluid Exit From Basolateral Spaces
6.3 Transjunctional Flows of Water and Ions
7 Role of Submucosa in Fluid Transport
7.1 Strength of Transport
8 Fluid Transport and Regulation of Cellular Volume
Figure 1. Figure 1.

Schematic drawing of an absorptive epithelial cell. Cell apical (mucosal) surface has microvilli; basal (serosal) surface exhibits infoldings. Na+ ‐K+ ‐ATPase is localized to the basolateral membrane; solute entry (generally NaCl) occurs across the apical membrane. Cells are joined by tight junctions at apical end of lateral intercellular spaces. Cells rest on a basement membrane and underlying connective tissue, which constitute subepithelial (submucosal) tissues.
Figure 2. Figure 2.

Diagram of Curran and MacIntosh 3‐compartment model for coupled solute‐water transport. Outer membrane has a high water permeability, relatively low solute permeability, and a near‐unity reflection coefficient for the solute. Inner membrane has high water and solute permeabilities and no solute reflection properties. Solute enters the middle compartment as result of transport by neighboring cells; water is then drawn by osmosis from outer bath across outer facing membrane. Influx of water increases hydrostatic pressure in the middle compartment, forcing water and solute out of the compartment across the inner membrane. Water will not leave across the outer membrane, because the hydrostatic pressure created is small in magnitude compared with the osmotic force generated by the solute concentration difference across this semipermeable membrane. Osmotic water flow does not occur across the inner membrane because of the lack of solute reflection by this barrier.
Figure 3. Figure 3.

Possible pathways for transepithelial water flow in a fluid‐transporting epithelium.
Figure 4. Figure 4.

Probable sequence of events in strength of transport experiment conducted in Necturus gallbladder. A: situation at time zero, the start of the experiment. Apical bath (M) has just been switched from control value of 200 mosmol/kg to 220 mosmol/kg by addition of an impermeant solute. Cell osmolality (202 mosmol/kg) and basolateral interstitial osmolality (203 mosmol/kg) are computed from rate of transepithelial fluid transport and membrane water permeabilities. Basal bathing solution (S) is always assumed to be at 200 mosmol/kg. Dotted area beneath cell, subepithelial connective tissues. Solid line at lower right, probable NaCl concentration profile across this subepithelial layer. Dashed arrow, water flow from cell to apical bath. B: situation 15 s later. Cell osmolality has risen to 210 mosmol/kg as a result of water flow from cell to apical bath. Interspace osmolality has not changed significantly. C: situation at peak of osmotically induced shrinkage of cell, 30 s after initial change. Cell osmolality now equals that of the apical bath, but basolateral interstitial osmolality is still rising and now equals 210 mosmol/kg. D: final steady‐state situation in which transepithelial fluid transport has ceased as result of disappearance of osmotic driving forces for water movement. Steep concentration gradient for NaCl from basolateral interstitium to serosal bath has developed. NaCl diffusion from basolateral space to serosal bath is sufficiently increased to prevent any significant buildup of NaCl in these spaces resulting from active solute extrusion.
Figure 5. Figure 5.

Idealized version of experiments performed on Necturus gallbladder epithelium (described in refs. 45 and 54). Ordinate, relative cell volume, expressed as percentage of experimental/control. At time zero, 10−4 M ouabain was added to the serosal bath to inhibit Na+‐K+‐ATPase. Cell swelling occurs at 4%/min. At 5 min, mucosal bath osmolality was reduced by 18%. Cell volume increases rapidly (30 s) as a result of osmotic water flow. Volume regulatory decrease occurs, and cell volume is restored to the value expected after ouabain treatment alone. Osmotically induced volume regulatory decrease does not result in a return to control volume but to the ouabain‐induced value.


Figure 1.

Schematic drawing of an absorptive epithelial cell. Cell apical (mucosal) surface has microvilli; basal (serosal) surface exhibits infoldings. Na+ ‐K+ ‐ATPase is localized to the basolateral membrane; solute entry (generally NaCl) occurs across the apical membrane. Cells are joined by tight junctions at apical end of lateral intercellular spaces. Cells rest on a basement membrane and underlying connective tissue, which constitute subepithelial (submucosal) tissues.



Figure 2.

Diagram of Curran and MacIntosh 3‐compartment model for coupled solute‐water transport. Outer membrane has a high water permeability, relatively low solute permeability, and a near‐unity reflection coefficient for the solute. Inner membrane has high water and solute permeabilities and no solute reflection properties. Solute enters the middle compartment as result of transport by neighboring cells; water is then drawn by osmosis from outer bath across outer facing membrane. Influx of water increases hydrostatic pressure in the middle compartment, forcing water and solute out of the compartment across the inner membrane. Water will not leave across the outer membrane, because the hydrostatic pressure created is small in magnitude compared with the osmotic force generated by the solute concentration difference across this semipermeable membrane. Osmotic water flow does not occur across the inner membrane because of the lack of solute reflection by this barrier.



Figure 3.

Possible pathways for transepithelial water flow in a fluid‐transporting epithelium.



Figure 4.

Probable sequence of events in strength of transport experiment conducted in Necturus gallbladder. A: situation at time zero, the start of the experiment. Apical bath (M) has just been switched from control value of 200 mosmol/kg to 220 mosmol/kg by addition of an impermeant solute. Cell osmolality (202 mosmol/kg) and basolateral interstitial osmolality (203 mosmol/kg) are computed from rate of transepithelial fluid transport and membrane water permeabilities. Basal bathing solution (S) is always assumed to be at 200 mosmol/kg. Dotted area beneath cell, subepithelial connective tissues. Solid line at lower right, probable NaCl concentration profile across this subepithelial layer. Dashed arrow, water flow from cell to apical bath. B: situation 15 s later. Cell osmolality has risen to 210 mosmol/kg as a result of water flow from cell to apical bath. Interspace osmolality has not changed significantly. C: situation at peak of osmotically induced shrinkage of cell, 30 s after initial change. Cell osmolality now equals that of the apical bath, but basolateral interstitial osmolality is still rising and now equals 210 mosmol/kg. D: final steady‐state situation in which transepithelial fluid transport has ceased as result of disappearance of osmotic driving forces for water movement. Steep concentration gradient for NaCl from basolateral interstitium to serosal bath has developed. NaCl diffusion from basolateral space to serosal bath is sufficiently increased to prevent any significant buildup of NaCl in these spaces resulting from active solute extrusion.



Figure 5.

Idealized version of experiments performed on Necturus gallbladder epithelium (described in refs. 45 and 54). Ordinate, relative cell volume, expressed as percentage of experimental/control. At time zero, 10−4 M ouabain was added to the serosal bath to inhibit Na+‐K+‐ATPase. Cell swelling occurs at 4%/min. At 5 min, mucosal bath osmolality was reduced by 18%. Cell volume increases rapidly (30 s) as a result of osmotic water flow. Volume regulatory decrease occurs, and cell volume is restored to the value expected after ouabain treatment alone. Osmotically induced volume regulatory decrease does not result in a return to control volume but to the ouabain‐induced value.

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Article Title: Mechanism of Fluid Transport by Epithelia
 

How to Cite

Kenneth R. Spring. Mechanism of Fluid Transport by Epithelia. Compr Physiol 2011, Supplement 19: Handbook of Physiology, The Gastrointestinal System, Intestinal Absorption and Secretion: 195-207. First published in print 1991. doi: 10.1002/cphy.cp060405