Glutamine transport in renal basolateral vesicles from dogs with metabolic acidosis

1984 ◽  
Vol 246 (1) ◽  
pp. F78-F86 ◽  
Author(s):  
D. W. Windus ◽  
D. E. Cohn ◽  
S. Klahr ◽  
M. R. Hammerman
Keyword(s):  
Metabolic Acidosis ◽  
Initial Rate ◽  
Basolateral Membrane ◽  
Cortical Cell ◽  
Membrane Vesicles ◽  
Ammonia Production ◽  
Basolateral Membrane Vesicles ◽  
Electrogenic Transport ◽  
Chronic Metabolic Acidosis ◽  
Glutamine Transport

To determine whether the increased ammonia production per nephron in chronic metabolic acidosis is accompanied by augmented L-glutamine transport across the basolateral membrane of the renal cortical cell and consequent increased availability of this ammoniagenic amino acid, we measured L-[3H]glutamine transport in basolateral membrane vesicles (BLMV) isolated from kidneys of normal and acidotic dogs. Na+ -dependent electrogenic transport of L-[3H]glutamine was demonstrated in BLMV from kidneys of normal dogs that exhibited saturability over the concentration range of 25 microM to 2 mM L-glutamine. The apparent Km was 416 +/- 114 microM and Vmax was 536 +/- 129 pmol X mg protein-1 X 15 s-1. The initial rate of Na+ -dependent L-[3H]glutamine transport was increased in BLMV from kidneys of acidotic dogs, as reflected by an increased apparent Vmax. We conclude that an adaptation resulting in greater uptake of L-glutamine across the basolateral membrane of the renal cortical cell may underlie, in part, the increased rate of ammonia production per nephron seen in chronic metabolic acidosis.

scholarly journals Effect of acidosis on glutamine transport by isolated rat renal brush-border and basolateral-membrane vesicles

1983 ◽  
Vol 212 (3) ◽  
pp. 713-720 ◽  
Author(s):  
J W Foreman ◽  
R A Reynolds ◽  
K Ginkinger ◽  
S Segal
Keyword(s):  
Brush Border ◽  
Initial Rate ◽  
Basolateral Membrane ◽  
High Capacity ◽  
Membrane Vesicles ◽  
Transport Systems ◽  
Basolateral Membrane Vesicles ◽  
Glutamine Transport ◽  
Glutamine Uptake ◽  
Renal Brush Border

Glutamine uptake was examined in isolated renal brush-border and basolateral-membrane vesicles from control and acidotic rats. In brush-border vesicles from acidotic animals, there was a significant increase in the initial rate of glutamine uptake compared with that in controls. Lowering the pH of the medium increased the initial rate of glutamine uptake in brush-border vesicles from acidotic, but not from control, rats. In brush-border vesicles from both groups of animals, two saturable transport systems mediated glutamine uptake. There was a 2-fold increase in the Vmax. of the low-affinity high-capacity system in the brush-border vesicles from the acidotic animals compared with that from control animals, with no alteration in the other kinetic parameters. There was no difference in glutamine uptake by the two saturable transport systems in basolateral vesicles from control and acidotic animals. Lowering the incubation-medium pH increased the uptake of glutamine by basolateral vesicles from both control and acidotic rats to a similar extent. The data indicate that during acidosis there are alterations in glutamine transport by both the basolateral and brush-border membrane which could enhance its uptake by the renal-tubule cell for use in ammoniagenesis.

scholarly journals Anion dependence of bumetanide binding and ion transport by the rabbit parotid Na+-K+-2CI− co-transporter: evidence for an intracellular anion modifier site

1995 ◽  
Vol 309 (2) ◽  
pp. 637-642 ◽  
Author(s):  
M L Moore ◽  
J N George ◽  
R J Turner
Keyword(s):  
Initial Rate ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Basolateral Membrane Vesicles ◽  
Binding Event ◽  
Biphasic Effect ◽  
Cytosolic Side ◽  
Inhibitory Site ◽  
Anion Site ◽  
Transport Site

The anion dependence of [3H]bumetanide binding and 22Na+ transport by the rabbit parotid Na(+)-K(+)-2Cl- co-transporter was studied in acinar basolateral membrane vesicles (BLMVs). Cl-, Br- and NO3- have a biphasic effect on binding consistent with the presence of two anion sites associated with the bumetanide binding event, a high-affinity stimulatory site and a lower-affinity inhibitory site. We show that formate shares only the stimulatory site and SO4(2-) only the inhibitory site. The initial rate of [3H]bumetanide binding was stimulated by formate or low [Cl-] and inhibited by SO4(2-) or high [Cl-], but the rate of [3H]bumetanide dissociation was not affected by the presence of these anions in the dissociation medium. However, when [3H]bumetanide was bound to BLMVs in the presence of formate its rate of dissociation was more than four times faster than when binding took place in the presence of Cl-. These observations indicate that the binding of bumetanide and the stimulatory anion are ordered such that the anion must necessarily bind first and subsequently cannot dissociate until after bumetanide dissociates. In zero-trans-flux experiments, extravesicular SO4(2-) and formate had no effect on 22Na+ transport via the co-transporter [Turner and George (1988) J. Membr. Biol. 102, 71-77]. Thus neither of the anion sites associated with bumetanide binding is a Cl- transport site. However, we show here that SO4(2-) inhibits transport when present in the intravesicular space. Since the BLMV preparation is predominantly oriented cytosolic-side-in, this observation indicates the existence of an inhibitory cytosolic anion modifier site. Our data suggest that this site is identical to the inhibitory anion site associated with bumetanide binding.

Glutamine transport in basolateral vesicles from dogs with acute respiratory acidosis

1984 ◽  
Vol 247 (3) ◽  
pp. F403-F407 ◽  
Author(s):  
D. W. Windus ◽  
S. Klahr ◽  
M. R. Hammerman
Keyword(s):  
Basolateral Membrane ◽  
Respiratory Acidosis ◽  
Membrane Vesicles ◽  
Proximal Tubular Cell ◽  
Tubular Cell ◽  
Basolateral Membrane Vesicles ◽  
Renal Proximal Tubular Cell ◽  
Glutamine Transport ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

It has been shown that acute respiratory acidosis in dogs results in enhanced renal extraction of L-glutamine from plasma and increased ammonia excretion per nephron. To determine whether a component of the enhanced L-glutamine extraction results from increased transport of L-glutamine across the basolateral membrane into the renal proximal tubular cell, we measured Na+ gradient-dependent L-[3H]glutamine transport in proximal tubular basolateral membrane vesicles isolated from kidneys of normal dogs and from kidneys of dogs following 2 h of acute respiratory acidosis. The initial rate of Na+ gradient-dependent L-[3H] glutamine uptake (15 s) was increased significantly in basolateral membrane vesicles from the acidotic compared with normal dogs. Increased uptake could be measured under conditions in which changes in membrane potential resulting from fluxes of solute were minimized. We conclude that an adaptation occurs in the basolateral membrane of the renal proximal tubular cell during acute respiratory acidosis that allows increased transport of L-glutamine across the membrane into the proximal tubular cell. This adaptation may permit increased ammonia production per nephron.

scholarly journals The use of potential-sensitive cyanine dye for studying ion-dependent electrogenic renal transport of organic solutes. Spectrophotometric measurements

1982 ◽  
Vol 208 (2) ◽  
pp. 359-368 ◽  
Author(s):  
Ulrich Kragh-Hansen ◽  
Karl Evald Jørgensen ◽  
M. Iqbal Sheikh
Keyword(s):  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Cyanine Dye ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Renal Transport ◽  
Organic Solutes ◽  
Basolateral Membrane Vesicles ◽  
Electrogenic Transport ◽  
Luminal Membrane

Renal transport of four different categories of organic solutes, namely sugars, neutral amino acids, monocarboxylic acids and dicarboxylic acids, was studied by using the potential-sensitive dye 3,3′-diethyloxadicarbocyanine iodide in purified luminal-membrane and basolateral-membrane vesicles isolated from rabbit kidney cortex. Valinomycin-induced K+ diffusion potentials resulted in concomitant changes in dye–membrane-vesicle absorption spectra. Linear relationships were obtained between these changes and depolarization and hyperpolarization of the vesicles. Addition of d-glucose, l-phenylalanine, succinate or l-lactate to luminal-membrane vesicles, in the presence of an extravesicular>intravesicular Na+ gradient, resulted in rapid transient depolarization. With basolateral-membrane vesicles no electrogenic transport of d-glucose or l-phenylalanine was observed. Spectrophotometric competition studies revealed that d-galactose is electrogenically taken up by the same transport system as that for d-glucose, whereas l-phenylalanine, succinate and l-lactate are transported by different systems in luminal-membrane vesicles. The absorbance changes associated with simultaneous addition of d-glucose and l-phenylalanine were additive. The uptake of these solutes was influenced by the presence of Na+-salt anions of different permeabilities in the order: Cl−>SO42−>gluconate. Addition of valinomycin to K+-loaded vesicles enhanced uptake of d-glucose and l-phenylalanine in the presence of an extravesicular>intravesicular Na+ gradient. Gramicidin or valinomycin plus nigericin diminished/abolished electrogenic solute uptake by Na+- or Na++K+-loaded vesicles respectively. These results strongly support the presence of Na+-dependent renal electrogenic transport of d-glucose, l-phenylalanine, succinate and l-lactate in luminal-membrane vesicles.

Glutamine transport by rat basolateral membrane vesicles

1989 ◽  
Vol 979 (1) ◽  
pp. 77-81 ◽  
Author(s):  
Fayez K. Ghishan ◽  
William Sutter ◽  
Hamid Said ◽  
Dan Leonard ◽  
John Pietsch ◽  
...  
Keyword(s):  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Basolateral Membrane Vesicles ◽  
Glutamine Transport

Depression of calcium pump activity in renal cortex of vitamin D-deficient rats with secondary hyperparathyroidism

1990 ◽  
Vol 123 (4) ◽  
pp. 438-444 ◽  
Author(s):  
Yusuke Tsukamoto ◽  
Teiichi Tamura ◽  
Michiyo Saitoh ◽  
Yumiko Takita ◽  
Toshiaki Nakano
Keyword(s):  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Hormonal Regulation ◽  
Serum Calcium Level ◽  
Renal Cortex ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Calcium Pump ◽  
Basolateral Membrane Vesicles ◽  
Pump Activity

Abstract. To examine the hormonal regulation of the ATP-dependent Ca2+ pump in the kidneys, the ATP-dependent Ca2+ uptake by the basolateral membrane vesicles in the renal cortex was measured using radioactive calcium (45Ca2+) in rats with vitamin D deficiency or rats undergoing thyroparathyroidectomy. The Vmax of the Ca2+ pump activity was increased not only by administering calcitriol, but also by normalizing the serum calcium level in vitamin D-deficient rats. PTH suppressed the Ca2+ pump activity in normocalcemic vitamin D-deficient rats. Thyroparathyroidectomy did not affect the Ca2+ pump activity in the kidneys of normal rats. It was concluded that the ATP-dependent Ca2+ pump activity was depressed by secondary hyperparathyroidism in vitamin D-deficient rats.

scholarly journals Characterization of sodium-dependent and sodium-independent nucleoside transport systems in rabbit brush-border and basolateral plasma-membrane vesicles from the renal outer cortex

1989 ◽  
Vol 264 (1) ◽  
pp. 223-231 ◽  
Author(s):  
T C Williams ◽  
A J Doherty ◽  
D A Griffith ◽  
S M Jarvis
Keyword(s):  
Brush Border ◽  
Basolateral Membrane ◽  
Membrane Vesicles ◽  
Nucleoside Transport ◽  
Transport Systems ◽  
Facilitated Diffusion ◽  
Basolateral Membrane Vesicles ◽  
Plasma Membrane Vesicles ◽  
Outer Cortex ◽  
Overshoot Phenomenon

The transport of uridine into rabbit renal outer-cortical brush-border and basolateral membrane vesicles was compared at 22 degrees C. Uridine was taken up into an osmotically active space in the absence of metabolism for both types of membrane vesicles. Uridine influx by brush-border membrane vesicles was stimulated by Na+, and in the presence of inwardly directed gradients of Na+ a transient overshoot phenomenon was observed, indicating active transport. Kinetic analysis of the saturable Na+-dependent component of uridine flux indicated that it was consistent with Michaelis-Menten kinetics (Km 12 +/- 3 microM, Vmax. 3.9 +/- 0.9 pmol/s per mg of protein). The sodium:uridine coupling stoichiometry was found to be consistent with 1:1 and involved the net transfer of positive charge. In contrast, uridine influx by basolateral membrane vesicles was not dependent on the cation present and was inhibited by nitrobenzylthioinosine (NBMPR). NBMPR-sensitive uridine transport was saturable (Km 137 +/- 20 microM, Vmax. 5.2 +/- 0.6 pmol/s per mg of protein). Inhibition of uridine flux by NBMPR was associated with high-affinity binding of NBMPR to the basolateral membrane (Kd 0.74 +/- 0.46 nM). Binding of NBMPR to these sites was competitively blocked by adenosine and uridine. These results indicate that uridine crosses the brush-border surface of rabbit proximal renal tubule cells by Na+-dependent pathways, but permeates the basolateral surface by NBMPR-sensitive facilitated-diffusion carriers.

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