Study of the mechanism by which the Na+-Pi co-transporter of mouse kidney proximal-tubule cells adjusts to phosphate depletion

Jahan, Mussarat; Butterworth, Peter J.

doi:10.1042/bj2520105

Cited by 12 publications

(4 citation statements)

References 16 publications

(16 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, phosphate uptake was carrier mediated since it was highly sensitive t o inhibition by the analogue arsenate. Our data concerning the characteristics of phosphate uptake are consistent with those previously described in LLC-PK, cells (a pig kidney cell line; Biber et al, 1983), and in primary renal cells of rabbit (Waqar et al, 1985) and mouse (Kinoshita et al, 1986;Bell et al, 1988;Jahan and Butterworth, 1988). This putative Naphosphate cotransporter has not been purified, but was recently identified in rat kidney brush border membrane by Pratt and Pedersen (1989).…”

Section: Discussionsupporting

confidence: 93%

Sodium‐dependent phosphate transport in primary cultures of renal tubule cells from young and adult rats

Chen

King

Armbrecht

1990

Journal Cellular Physiology

View full text Add to dashboard Cite

The transport of phosphate by primary cultures of renal cells from young (5-6 weeks) and adult (10-12 months) rats was studied. Renal tubule cells isolated from young and adult groups exhibited typical epithelial morphology and similar growth rates. The Na-dependent phosphate uptake was saturable with a Km of 5-7 microM over a substrate range of 1-500 microM. A decrease in Na-dependent phosphate uptake in adult cells (30%) was found compared to that of young cells. The Na-independent component of phosphate uptake did not vary with age. In addition, the inhibition of phosphate uptake by a variety of compounds (ouabain, gramicidin, 2,4-dinitrophenol, KCN, and arsenate) were similar in both age groups. Kinetic analysis showed that a significant reduction in Vmax (4.4 +/- 0.4 vs. 3.1 +/- 0.2 nmol Pi/mg protein/10 min in young and adult cells, respectively), but not Km, resulted in this decreased uptake of phosphate in adult groups. There was no difference in the efflux of phosphate from both age groups. When cells were preincubated in a phosphate-free medium for 24 hours, the uptake of phosphate was increased to 46% and 24% of their corresponding controls in young and adult cells, respectively. The decreased phosphate uptake and limited adaptation to a phosphate-free medium by the adult renal cells may account for the hypophosphatemia and phosphaturia seen in adult and old animals in vivo.

show abstract

Section: Discussionsupporting

confidence: 93%

Sodium‐dependent phosphate transport in primary cultures of renal tubule cells from young and adult rats

Chen

King

Armbrecht

1990

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…lb and 2b) strikingly resembles time courses reported in washed cells [9,10,26]. Furthermore, a recent study of renal epithelial cells, with no washing step, has demonstrated a rapid phase of labelling at low temperature, which was not attributed to trapped extracellular medium [29].…”

Section: Labelling Of Cellular Pisupporting

confidence: 64%

“…Even though the contribution from trapped extra-48 cellular medium, which contains I mM-Pi, was subtracted here in all measurements, the fast-labelling Pi pool could be bound to the cell surface, although the binding would need to be weak (Km approx. millimolar) to account for the doubling of the pool when the extracellular Pi concentration was doubled (Table 2 and [29]). Such binding would be surprising in view of the net negative charge on the membrane, but a Pi pool associated with the cytosolic face of the plasma membrane has been reported in pancreatic fl-cells [30].…”

Section: Labelling Of Cellular Pimentioning

confidence: 99%

32P-labelling anomalies in human erythrocytes. Is there more than one pool of cellular Pi?

Kemp

Bevington

Khodja

et al. 1989

Biochemical Journal

View full text Add to dashboard Cite

1. Human erythrocytes were incubated in autologous plasma containing [32P]Pi, and sampled by a method which avoids washing the cells. 2. In experiments of up to 3 h duration, the specific radioactivity of cellular Pi stabilized at a value below that of extracellular Pi. This can be explained on the basis of a single cellular Pi pool exchanging with a large unlabelled pool of cellular organic phosphates. 3. However, a rapid initial phase of labelling, occurring within 30 s, was inconsistent with the situation described in point 2. A possible explanation is that about 1/4 of cellular Pi occurs in a separate, fast-labelling pool. 4. When the extracellular Pi concentration was doubled, most of the corresponding increase in the steady-state cellular Pi concentration was accounted for by the apparent fast-labelling Pi pool, which also doubled. 5. The observed initial rate of labelling of cellular organic phosphates [which probably occurs through the reaction catalysed by glyceraldehyde-3-phosphate dehydrogenase (E.C. 1.2.1.12)] was considerably lower than that predicted from the flux through the Embden-Meyerhof pathway. This implies that the enzyme is exposed to Pi whose specific radioactivity is lower than the mean specific radioactivity of cellular Pi, and fails to support earlier suggestions that this enzyme uses extracellular Pi. 6. In 3 h incubations, the rate of organic phosphate labelling was roughly constant throughout, even though the specific radioactivity of cellular Pi had risen slowly to a plateau. Viewed in conjunction with point 5, this again suggests some inhomogeneity in cellular Pi. 7. Cellular Pi and extracellular Pi only reached isotopic steady state after 2 days. At this stage some organic phosphates were probably still incompletely labelled. 8. We conclude that, whatever their physical or technical reasons, such labelling inhomogeneities and slow attainment of isotopic steady state may cause serious misinterpretation of results if ignored during 32P-labelling of intact cells.

show abstract

“…Low phosphate dietary intake stimulates intestinal and renal NaPi co-transporters expression leading to increased absorption of phosphate from the intestine and reabsorption from the proximal tubules (Danisi et al, 1990, Katai et al, 1999, Stoll et al, 1979, Jahan and Butterworth, 1988). In addition, low phosphate induces an increase in circulating 1α, 25(OH) 2 D 3 (Danisi et al, 1990).…”

Section: Factors Affecting Phosphate Homoeostasismentioning

confidence: 99%

Hyperphosphatemia Management in Patients with Chronic Kidney Disease

Shaman

Kowalski

2016

Saudi Pharmaceutical Journal

View full text Add to dashboard Cite

Hyperphosphatemia in chronic kidney disease (CKD) patients is a potentially life altering condition that can lead to cardiovascular calcification, metabolic bone disease (renal osteodystrophy) and the development of secondary hyperparathyroidism (SHPT). It is also associated with increased prevalence of cardiovascular diseases and mortality rates. To effectively manage hyperphosphatemia in CKD patients it is important to not only consider pharmacological and nonpharmacological treatment options but also to understand the underlying physiologic pathways involved in phosphorus homoeostasis. This review will therefore provide both a background into phosphorus homoeostasis and the management of hyperphosphatemia in CKD patients. In addition, it will cover some of the most important reasons for failure to control hyperphosphatemia with emphasis on the effect of the gastric pH on phosphate binders efficiency.

show abstract

Study of the mechanism by which the Na+-Pi co-transporter of mouse kidney proximal-tubule cells adjusts to phosphate depletion

Cited by 12 publications

References 16 publications

Sodium‐dependent phosphate transport in primary cultures of renal tubule cells from young and adult rats

Sodium‐dependent phosphate transport in primary cultures of renal tubule cells from young and adult rats

32P-labelling anomalies in human erythrocytes. Is there more than one pool of cellular Pi?

Hyperphosphatemia Management in Patients with Chronic Kidney Disease

Contact Info

Product

Resources

About