Role of lateral intercellular space and sodium recirculation for isotonic transport in leaky epithelia

2008 ◽  
pp. 153-212 ◽  
Author(s):  
E. H. Larsen ◽  
S. Nedergaard ◽  
H. H. Ussing
Keyword(s):  
Intercellular Space ◽  
Leaky Epithelia ◽  
Lateral Intercellular Space

Water permeability and pathways in the proximal tubule

1983 ◽  
Vol 245 (3) ◽  
pp. F279-F294 ◽  
Author(s):  
C. A. Berry
Keyword(s):  
Proximal Tubule ◽  
Water Transport ◽  
Water Permeability ◽  
Intercellular Space ◽  
Proximal Convoluted Tubule ◽  
Pressure Gradients ◽  
Solvent Drag ◽  
Lateral Intercellular Space ◽  
Volume Absorption ◽  
Osmotic Water

The route of water transport in the proximal tubule could be either transjunctional or transcellular. A transjunctional route is supported by data showing high osmotic-to-diffusive water permeability ratios, the possible correlation of junctional leakiness to ions and nonelectrolytes with water permeability, and solvent drag of nonelectrolytes and ions. These data, however, are not convincing. A transcellular route of water transport is supported by data showing that the osmotic water permeability (Pf) for apical and/or basolateral cell membranes is sufficiently high to account for the transepithelial Pf, making a tentative conclusion for a transcellular route of water transport possible. In addition, measurements of Pf have yielded insights into the mechanism of solute-solvent coupling. Pf has been reported to be mostly between 0.1 and 0.3 cm/s. In the rabbit proximal straight and the Necturus proximal convoluted tubule, in which water transport rates are low, this range of Pf will account for volume absorption with only small osmotic gradients (less than 6 mosmol). Higher osmotic gradients are required in the rat and possibly the rabbit proximal convoluted tubule, where water transport rates are higher. Solute-solvent coupling in all species is probably due to both luminal hypotonicity and lateral intercellular space hypertonicity. These two processes are directly linked. Mass balance requires that generation of luminal hypotonicity also generates a hypertonic absorbate and, thus, some degree of lateral intercellular space hypertonicity. It is likely that, in the rabbit at least, effective osmotic pressure gradients due to differences in solute reflection coefficients play little role in solute-solvent coupling.

The lateral intercellular space as osmotic coupling compartment in isotonic transport

2009 ◽  
Vol 195 (1) ◽  
pp. 171-186 ◽  
Author(s):  
E. H. Larsen ◽  
N. J. Willumsen ◽  
N. Møbjerg ◽  
J. N. Sørensen
Keyword(s):  
Intercellular Space ◽  
Lateral Intercellular Space

Effects of Depth of Flooding on Growth and Anatomy of Stems and Knee Roots of Taxodium Distichum

IAWA Journal ◽  
1992 ◽  
Vol 13 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Fukuju Yamamoto
Keyword(s):  
Intercellular Space ◽  
Height Growth ◽  
Taxodium Distichum ◽  
Diameter Growth ◽  
Xylem Anatomy ◽  
Flood Water ◽  
Inner Bark

Depth of flooding of Taxodium distichum trees influeneedin height and diametergrowth, formation of knee roots , and anatomy of sterns and knee roots. Height growth was progressively redueed and diameter growth was inereased as the level of the flood water was inereased. Formation of knee roots deereased as the depth of flooding inereased. Traeheids in the submerged portions of sterns of deeply flooded trees were shorter, slightly wider, and had thinner walls than traeheids of shallowly flooded trees. The inner bark of the submerged sterns of deeply flooded trees had wider phloemrays and more intercellular space than the bark of shallowly flooded trees. The xylem anatomy of knee roots resembled that of the xylem in the submerged portions of sterns of deeply flooded trees. Flooding stimulated ethylene produetion by stern bark and apieal portions of knee roots. An interaetive role of ethylene and auxin in anatomical responses of Taxodium to the flooding is postulated.

scholarly journals Occluding junctions and paracellular pathways studied in monolayers of MDCK cells

1983 ◽  
Vol 106 (1) ◽  
pp. 205-215 ◽  
Author(s):  
M. Cereijido ◽  
L. Gonzalez-Mariscal ◽  
L. Borboa
Keyword(s):  
Electrical Resistance ◽  
Intercellular Space ◽  
Mdck Cells ◽  
Freeze Fracture ◽  
Apical Surface ◽  
Leaky Epithelia ◽  
Occluding Junctions ◽  
Freeze Fracture Electron Microscopy ◽  
Current Flows ◽  
High Conductance

MDCK cells (epithelioid, derived from the kidney of a normal dog) cultured in monolayers on a permeable support, exhibit properties of natural transporting epithelia. Comparisons of the electrical resistance across the plasma membrane of MDCK cells (as studied with microelectrodes) and the resistance across the whole monolayer, (mounted as a flat sheet between two chambers) indicate that most of the current flows through an extracellular pathway. Scanning of the electrical field over the apical surface shows that this pathway is located at the intercellular space. Yet conductance is not evenly distributed along the intercellular space as in leaky epithelia, but is restricted to sites scattered irregularly along the intercellular space. Studies of freeze fracture electron microscopy indicate that the number of strands of the junctions is also distributed irregularly, varying from 1 to 10 in a few nanometers. This suggests that regions with few strands would correspond to spots with high conductance and vice versa. However, in this preparation the sealing property of the junction bears little relationship to its structure. Thus by changing the temperature from 37 to 3 degrees C and back, the electrical resistance increases reversibly by 306%, while the number and arrangement of the strands show no significant modification. The resistance of the monolayer varies also with the age of the cells, suggesting that sealing and ion-permeating components of the junction may be dynamic entities that are not permanently installed, but can be accommodated to the requirements of the tissue.

Regulation of Light Energy Distribution between Photosynthetic Pigment Systems; a Possible Role of Leaf Anatomy

1983 ◽  
Vol 38 (7-8) ◽  
pp. 600-603 ◽  
Author(s):  
G. Hamischfeger ◽  
G. Zenk
Keyword(s):  
Light Absorption ◽  
Energy Flow ◽  
Intercellular Space ◽  
Photosynthetic Pigment ◽  
Anatomical Structure ◽  
Higher Plant ◽  
Long Wavelength ◽  
Isolated Chloroplasts ◽  
Secondary Fluorescence

The complex anatomical structure of an intact leaf results in a distribution of photosynthetically active energy between photosynthetic pigments which is different from that observed in isolated chloroplasts. The variance is due mainly to scattering at the gas-liquid interface between cells and intercellular space which tends to increase light absorption by the long wavelength absorbing pigments through secondary fluorescence. Evidence is given in support of an active use of this feature by the higher plant to regulate energy flow at the photophysical level of light absorption.

NO increases permeability of cultured human cervical epithelia by cGMP-mediated increase in G-actin

2000 ◽  
Vol 278 (5) ◽  
pp. C942-C952 ◽  
Author(s):  
George I. Gorodeski
Keyword(s):  
Protein Kinase ◽  
Cell Size ◽  
Guanylate Cyclase ◽  
Intercellular Space ◽  
Paracellular Permeability ◽  
Dependent Protein Kinase ◽  
Lateral Intercellular Space ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein ◽  
Ly 83583

Human cervical epithelial cells express mRNA for the nitric oxide (NO) synthase (NOS) isoforms ecNOS, bNOS, and iNOS and release NO into the extracellular medium. NG-nitro-l-arginine methyl ester (l-NAME), an NOS inhibitor, and Hb, an NO scavenger, decreased paracellular permeability; in contrast, the NO donors sodium nitroprusside (SNP) and N-(ethoxycarbonyl)-3-(4-morpholinyl)sydnonimine increased paracellular permeability across cultured human cervical epithelia on filters, suggesting that NO increases cervical paracellular permeability. The objective of the study was to understand the mechanisms of NO action on cervical paracellular permeability. 8-Bromo-cGMP (8-BrcGMP) also increased permeability, and the effect was blocked by KT-5823 (a blocker of cGMP-dependent protein kinase), but not by LY-83583 (a blocker of guanylate cyclase). In contrast, LY-83583 and KT-5823 blocked the SNP-induced increase in permeability. Treatment with SNP increased cellular cGMP, and the effect was blocked by Hb and LY-83583, but not by KT-5823. Neither SNP nor 8-BrcGMP had modulated cervical cation selectivity. In contrast, both agents increased fluorescence from fura 2-loaded cells in the Ca2+-insensitive wavelengths, indicating that SNP and 8-BrcGMP stimulate a decrease in cell size and in the resistance of the lateral intercellular space. Neither SNP nor 8-BrcGMP had an effect on total cellular actin, but both agents increased the fraction of G-actin. Hb blocked the SNP-induced increase in G-actin, and KT-5823 blocked the 8-BrcGMP-induced increase in G-actin. On the basis of these results, it is suggested that NO acts on guanylate cyclase and stimulates an increase in cGMP; cGMP, acting via cGMP-dependent protein kinase, shifts actin steady-state toward G-actin; this fragments the cytoskeleton and renders cells more sensitive to decreases in cell size and resistance of the lateral intercellular space and, hence, to increases in permeability. These results may be important for understanding NO regulation of transcervical paracellular permeability and secretion of cervical mucus in the woman.

scholarly journals Fluid Transport Across Leaky Epithelia: Central Role of the Tight Junction and Supporting Role of Aquaporins

2010 ◽  
Vol 90 (4) ◽  
pp. 1271-1290 ◽  
Author(s):  
Jorge Fischbarg
Keyword(s):  
Tight Junction ◽  
Corneal Endothelium ◽  
Fluid Transport ◽  
Regulatory Volume Decrease ◽  
Electrical Currents ◽  
Leaky Epithelia ◽  
Local Osmosis ◽  
Electro Osmosis ◽  
Volume Decrease

The mechanism of epithelial fluid transport remains unsolved, which is partly due to inherent experimental difficulties. However, a preparation with which our laboratory works, the corneal endothelium, is a simple leaky secretory epithelium in which we have made some experimental and theoretical headway. As we have reported, transendothelial fluid movements can be generated by electrical currents as long as there is tight junction integrity. The direction of the fluid movement can be reversed by current reversal or by changing junctional electrical charges by polylysine. Residual endothelial fluid transport persists even when no anions (hence no salt) are being transported by the tissue and is only eliminated when all local recirculating electrical currents are. Aquaporin (AQP) 1 is the only AQP present in these cells, and its deletion in AQP1 null mice significantly affects cell osmotic permeability (by ∼40%) but fluid transport much less (∼20%), which militates against the presence of sizable water movements across the cell. In contrast, AQP1 null mice cells have reduced regulatory volume decrease (only 60% of control), which suggests a possible involvement of AQP1 in either the function or the expression of volume-sensitive membrane channels/transporters. A mathematical model of corneal endothelium we have developed correctly predicts experimental results only when paracellular electro-osmosis is assumed rather than transcellular local osmosis. Our evidence therefore suggests that the fluid is transported across this layer via the paracellular route by a mechanism that we attribute to electro-osmotic coupling at the junctions. From our findings we have developed a novel paradigm for this preparation that includes 1) paracellular fluid flow; 2) a crucial role for the junctions; 3) hypotonicity of the primary secretion; and 4) an AQP role in regulation rather than as a significant water pathway. These elements are remarkably similar to those proposed by the laboratory of Adrian Hill for fluid transport across other leaky epithelia.

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