scholarly journals Compensatory Regeneration as a Mechanism for Renal Tubule Carcinogenesis of Fumonisin B 1 in the F344/N/Nctr BR Rat

2001 ◽  
Vol 109 ◽  
pp. 309 ◽  
Author(s):  
Paul C. Howard ◽  
Alan Warbritton ◽  
Kenneth A. Voss ◽  
Ronald J. Lorentzen ◽  
J. Dale Thurman ◽  
...  
Keyword(s):  
Renal Tubule ◽  
Compensatory Regeneration

scholarly journals Compensatory regeneration as a mechanism for renal tubule carcinogenesis of fumonisin B1 in the F344/N/Nctr BR rat.

2001 ◽  
Vol 109 (suppl 2) ◽  
pp. 309-314 ◽  
Author(s):  
P C Howard ◽  
A Warbritton ◽  
K A Voss ◽  
R J Lorentzen ◽  
J D Thurman ◽  
...  
Keyword(s):  
Renal Tubule ◽  
Fumonisin B1 ◽  
Compensatory Regeneration

scholarly journals Exploration of the Basolateral Chloride Channels in the Renal Tubule using

2005 ◽  
Vol 99 (2) ◽  
pp. p64-p68 ◽  
Author(s):  
Jacques Teulon ◽  
Stéphane Lourdel ◽  
Antoine Nissant ◽  
Marc Paulais ◽  
Romain Guinamard ◽  
...  
Keyword(s):  
Chloride Channels ◽  
Renal Tubule

scholarly journals Therapeutic concentrations of cyclosporine A, but not FK506, increase P-glycoprotein expression in endothelial and renal tubule cells

1998 ◽  
Vol 54 (4) ◽  
pp. 1139-1149 ◽  
Author(s):  
Ingeborg A. Hauser ◽  
Michael Koziolek ◽  
Ulrich Hopfer ◽  
Frank Thévenod
Keyword(s):  
Cyclosporine A ◽  
Renal Tubule ◽  
P Glycoprotein ◽  
Tubule Cells

Applied physiology: the renal tubule

2001 ◽  
Vol 11 (3) ◽  
pp. 207-211
Author(s):  
C.J. Lote
Keyword(s):  
Renal Tubule ◽  
Applied Physiology

FLOW OF THE ELLIS FLUID IN THE RENAL TUBULE

2021 ◽  
Vol 62 (2) ◽  
pp. 292-299
Author(s):  
M. Sajid ◽  
M. Rooman ◽  
N. Ali ◽  
M. N. Sadiq
Keyword(s):  
Renal Tubule

Reversed polarity of Na(+) -K(+) -ATPase: mislocation to apical plasma membranes in polycystic kidney disease epithelia

1991 ◽  
Vol 260 (3) ◽  
pp. F420-F430 ◽  
Author(s):  
P. D. Wilson ◽  
A. C. Sherwood ◽  
K. Palla ◽  
J. Du ◽  
R. Watson ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Plasma Membranes ◽  
Renal Tubule ◽  
Apical Membrane ◽  
Membrane Vesicles ◽  
Renal Tubules ◽  
Polycystic Kidney ◽  
Permeable Membrane ◽  
Reversed Polarity

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder in which renal tubules become enormously enlarged due to fluid accumulation. Na(+) -K(+) -ATPase was compared in normal and cystic regions of whole kidneys and in confluent primary cultures of microdissected renal tubule and cyst-lining epithelia. Immunostaining with antibodies directed against the Na(+) -K(+) -ATPase catalytic alpha-subunit was confined to apical, luminal plasma membranes of ADPKD epithelia, which was a complete reversal of the normal renal tubule polarized location in basolateral membranes. Mislocated Na(+) -K(+) -ATPase was shown to be functionally active, because identical intense apical staining was observed by use of a cytochemical assay. In addition, biochemical assays showed a significant increase in these ouabain-inhibitable Na(+) -K(+) -ATPase specific activity levels in ADPKD kidneys compared with age-matched normal kidneys. Specific binding of [3H] ouabain was not only increased but also confined to the apical membrane vesicles prepared from cystic regions of ADPKD kidneys compared with normal age-matched controls, in which binding was confined to basolateral membrane vesicles. Although steady-state levels of Na(+) -K(+) -ATPase alpha- and beta-subunit in mRNAs were increased somewhat in ADPKD kidneys, this alone was not sufficient to account for the observed activation. Confluent ADPKD epithelia grown on dual-chamber, permeable membrane supports also showed reversed polarity of 22NaCl vectorial transport, because this was from basal to apical media compartments. Because this transport could also be blocked by ouabain, this suggested apical Na(+) -K(+) -ATPase was responsible and implicated altered polarity of Na(+) -K(+) -ATPase and resultant Na+ secretion as a mechanism for cyst formation in ADPKD. Because no reversal of polarity of other basolateral or apical membrane proteins was detected, an intracellular sorting defect specific for Na(+) -K(+) -ATPase is proposed.

Effect of ionophore RO 2-2985 on the efflux of calcium from the rat nephron

1978 ◽  
Vol 235 (4) ◽  
pp. F381-F384 ◽  
Author(s):  
H. O. Senekjian ◽  
T. F. Knight ◽  
A. Ince ◽  
E. J. Weinman
Keyword(s):  
Proximal Tubule ◽  
Sodium Phosphate ◽  
Orthophosphoric Acid ◽  
Renal Tubule ◽  
Specific Effect ◽  
Early Proximal Tubule

The effect of the ionophore RO 2-2985 on the efflux of calcium from the renal tubule was studied employing the in vivo microinjection technique. Microinjection solutions contained either RO 2-2985 (E) or its diluent (C). Following microinjections into the early proximal tubule, urinary 45Ca recoveries averaged 10.1 +/- 1.9 (C) and 3.5 +/- 1.4% (E) (P is less than 0.005), while recoveries averaged 32.3 +/- 6.9 (C) and 24.9 +/- 6.5% (E) (P is less than 0.05) following microinjections into the late proximal tubule. To determine if the decreased recovery of calcium was a specific effect, the effect of RO 2-2985 on the efflux of sodium, phosphate, and 3-O-methyl-D-glucose was examined. Compared to controls, RO2-2985 did not affect the urinary recoveries of 22Na, [32P]orthophosphoric acid, or 3-O-methyl-D-[14C]glucose. These studies demonstrate that RO 2-2985 enhances the efflux of calcium microinjected into the proximal portions of the rat nephron.

Effect of basement membrane and colloid osmotic pressure on renal tubule cell volume

1977 ◽  
Vol 233 (4) ◽  
pp. F325-F332
Author(s):  
M. A. Linshaw ◽  
F. B. Stapleton ◽  
F. E. Cuppage ◽  
J. J. Grantham
Keyword(s):  
Basement Membrane ◽  
Osmotic Pressure ◽  
Cell Volume ◽  
Cell Size ◽  
Renal Tubule ◽  
Colloid Osmotic Pressure ◽  
Outer Diameter ◽  
Tubule Cell ◽  
Cation Pump ◽  
Renal Tubule Cell

Renal tubule cell volume is thought to be kept constant by a cation pump. When active transport is blocked, intracellular impermeant solutes cause cells to swell. Cell size is then determined by transmembrane hydrostatic and colloid osmotic forces. We studied the importance of passive transmembrane forces in determining cell size in isolated rabbit proximal straight tubules (PST). We blocked active solute transport with ouabain and evaluated subsequent changes in cell size by measuring outer diameter of nonperfused tubules. Tubules in a ouabain and 6 g/100 ml protein bath swelled only 40% above control. However, removal of the tubule basement membrane with collagenase dissipated a transmembrane hydrostatic pressure and caused more swelling. Final cell volume was determined largely by bath protein concentration. Tubules in ouabain and collagenase swelled enormously in hyponcotic protein, moderately in isoncotic protein, and could be shrunk below control in hyperoncotic protein. Intracellular colloid osmotic pressure was estimated to exceed 38 cmH20. We conclude that hydrostatic and colloid osmotic forces are major determinants of cell size in isolated PST treated with ouabain.

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