The Polarity of the Proximal Tubule Cell in Rat Kidney

Heidrich, Hans-G.; Kinne, Rolf; Kinne-Saffran, Evamaria; Hannig, Kurt

doi:10.1083/jcb.54.2.232

Cited by 217 publications

(46 citation statements)

References 13 publications

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“…In fact, the inhibition of the transport enzyme Na-K-ATPase (30) suggests the occurrence of a defective ATP synthesis. In our study, major membranous changes were seen at the base of the cell where the Na-K-ATPase involved in active transport is localized (31)(32)(33)(34). While the brush border structure of the proximal nephron appeared to be well preserved (28,29) (35), who showed that maleic anhydride reacts rapidly and specifically with amino groups associated with the protein fraction of the red cell membrane.…”

Section: Introductionmentioning

confidence: 80%

Membrane permeability as a cause of transport defects in experimental Fanconi syndrome. A new hypothesis.

Bergeron¹,

Dubord²,

Hausser³

et al. 1976

J. Clin. Invest.

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A B S T R A C T The injection of sodium maleate (200-400 mg/kg) into rats produces aminoaciduria along with glycosuria and phosphaturia, resembling the Fanconi syndrome. This experimental model was studied by means of microinjections into proximal convoluted tubules of the kidney, stop-flow diuresis, and microperfusion of single nephrons. Our results show that, in maleate-treated rats, competition between amino acids of related structures (L-proline, L-OH-proline, and glycine) possesses the same characteristics, and net influx of amino acids appear normal at the proximal nephron. Data obtained by classical stop-flow techniques and single nephron microperfusions also indicate a normal entry of labeled amino acids (L-lysine, glycine, L-valine, L-proline, L-cystine), and 3-0-methyl-D-[3H]glucose and ['P]phosphate from the luminal side of the proximal tubule cell. However, the efflux of molecules from the cell appears enhanced throughout the proximal and distal tubule; molecules that exit at this site are excreted directly into the urine. Our results suggest that the phosphaturia, aminoaciduria, and glycosuria of the experimental Fanconi syndrome can be explained by a modification of the cell membrane permeability (increased efflux) at distal sites of the nephron rather than by a modification of the membrane transport (decreased influx) at the proximal sites, as is currently accepted. Our data also stress the importance of efflux phenomena in membrane transport.

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Section: Introductionmentioning

confidence: 80%

Membrane permeability as a cause of transport defects in experimental Fanconi syndrome. A new hypothesis.

Bergeron¹,

Dubord²,

Hausser³

et al. 1976

J. Clin. Invest.

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“…Cytochemical studies have indicated enzymic polarity on the cell surface of intestinal epithelial cells (Nachlas et al, 1960), kidney, pancreas and mammary-gland cells (de-The, 1968). Plasmamembrane subfractions that represent the resolution of this polarity to varying degrees have been prepared from intestinal epithelium (Fujita et al, 1973), kidney proximal tubule (Heidrich et al, 1972), the electroplax organ (Duguid & Raftery, 1973), blood platelets (Barber & Jamieson, 1970) and cultured hepatocytes (Perdue et al, 1971).…”

Section: Bile-canicularfacementioning

confidence: 99%

Functional polarity of the rat hepatocyte surface membrane. Isolation and characterization of plasma-membrane subfractions from the blood-sinusoidal, bile-Canalicular and contiguous surfaces of the hepatocyte

Wisher¹,

Evans²

1975

Biochemical Journal

305

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1. Six rat liver plasma-membrane subfractions of different density and morphological, enzymric and chemical properties were prepared from homogenates by a combination of differential, rate-zonal and density-gradient centrifugation. They consisted of three vesicular 'light' subfractions of density 1.12-1.13 and three 'heavy' subfractions of density 1.16-1.18 containing membrane strips and intercellular junctions. 2. All six subfractions contained a basal adenylate cyclase activity. One of the 'light' subfractions that showed the highest glucagon-stimulated adenylate cyclase activity was identified as deriving from the blood-sinusoidal face of the hepatocyte. This subfraction, unlike the others, was contaminated by Golgi components, as indicated by its morphological properties and the presence of galactosyl-and sialyl-transferase activities. 3. All the six subfractions showed high activities of the following plasma-membrane marker enzymes: 5'-nucleotidase, alkaline phosphodiesterase (nucleotide pyrophosphatase), alkaline phosphatase, leucine naphthylamidase and Mg2+-activated adenosine triphosphatase. A 'light' subfraction that showed the highest specific activities of all the above marker enzymes, but lacked a glucagon-stimulated adenylate cyclase activity, was identified as deriving from the bilecanalicular face of the hepatocyte. 4. The 'heavy' subfractions, which showed generally the lowest activities of the above plasma-membrane enzyme markers, and were characterized by the presence of desmosomes and gap junctions, were taken to originate from the contiguous faces of the hepatocyte. 5. The protein composition of the six subfractions was generally similar, as shown by polyacrylamide-gel electrophoresis. Differences in the amounts of various protein and glycoprotein bands among the subfractions correlated with their morphology, enzymic composition and sialic acid content. 6. Hormonal and histochemical evidence supporting the identification of a bile-canalicular subfraction, a blood-sinusoidal subfraction and contiguous-face subfractions is discussed.

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“…The kidney tissue from male Sprague-Dawley rats (300 g) was homogenized and fractionated according to the scheme in [4] up to the pre-free flow electrophoresis stage (fraction Ps). Homogenization buffer consisted of 10 mM triethanolamine-HCl (pH 7.5) containing 0.25 M sucrose (TS buffer).…”

Section: Resultsmentioning

confidence: 99%

Rapid purification of rat kidney brush borders enriched in γ‐glutamyl transpeptidase

1979

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The Polarity of the Proximal Tubule Cell in Rat Kidney

Cited by 217 publications

References 13 publications

Membrane permeability as a cause of transport defects in experimental Fanconi syndrome. A new hypothesis.

Membrane permeability as a cause of transport defects in experimental Fanconi syndrome. A new hypothesis.

Functional polarity of the rat hepatocyte surface membrane. Isolation and characterization of plasma-membrane subfractions from the blood-sinusoidal, bile-Canalicular and contiguous surfaces of the hepatocyte

Rapid purification of rat kidney brush borders enriched in γ‐glutamyl transpeptidase

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