Cellular mechanisms of inorganic phosphate transport in kidney

1986 ◽  
Vol 66 (1) ◽  
pp. 36-70 ◽  
Author(s):  
P. Gmaj ◽  
H. Murer
2021 ◽  
Vol 22 (11) ◽  
pp. 5701
Author(s):  
Lucile Figueres ◽  
Sarah Beck-Cormier ◽  
Laurent Beck ◽  
Joanne Marks

Phosphate homeostasis is essential for health and is achieved via interaction between the bone, kidney, small intestine, and parathyroid glands and via intricate processes involving phosphate transporters, phosphate sensors, and circulating hormones. Numerous genetic and acquired disorders are associated with disruption in these processes and can lead to significant morbidity and mortality. The role of the kidney in phosphate homeostasis is well known, although it is recognized that the cellular mechanisms in murine models and humans are different. Intestinal phosphate transport also appears to differ in humans and rodents, with recent studies demonstrating a dominant role for the paracellular pathway. The existence of phosphate sensing has been acknowledged for decades; however, the underlying molecular mechanisms are poorly understood. At least three phosphate sensors have emerged. PiT2 and FGFR1c both act as phosphate sensors controlling Fibroblast Growth Factor 23 secretion in bone, whereas the calcium-sensing receptor controls parathyroid hormone secretion in response to extracellular phosphate. All three of the proposed sensors are expressed in the kidney and intestine but their exact function in these organs is unknown. Understanding organ interactions and the mechanisms involved in phosphate sensing requires significant research to develop novel approaches for the treatment of phosphate homeostasis disorders.


1963 ◽  
Vol 205 (1) ◽  
pp. 107-111 ◽  
Author(s):  
Harold E. Harrison ◽  
Helen C. Harrison

Everted loops of rat small intestine were incubated in media varying in their concentrations of sodium and potassium. Reduction of sodium concentration was effected by substitution of choline chloride in equimolar amounts for sodium chloride in the saline-bicarbonate buffer. Concentrative transport of glucose, l-tyrosine, inorganic phosphate, and calcium was measured by determination of the final ratio of the concentrations of the solute in serosal and mucosal fluids, and the increment of the solute in serosal fluid during incubation. Ca45 was used as an indicator of calcium distribution. The glucose, l-tyrosine, and inorganic phosphate transport systems require sodium, and at a submaximal concentration of sodium an increased concentration of potassium is inhibitory. The calcium transport system does not require sodium and in loops from the distal small intestine calcium transport is enhanced by reduction of sodium concentration in the medium. It is postulated that there is a common sodium-requiring system which is necessary for the linkage of metabolic energy to glucose, amino acid, and inorganic phosphate transport.


1955 ◽  
Vol 33 (1) ◽  
pp. 638-650 ◽  
Author(s):  
James G. Foulks

By means of the infusion of small amounts of sodium sulphate it has been possible to elevate the filtered load of inorganic phosphate to the renal tubule in fasted dogs without the administration of exogenous phosphate. Under these circumstances, the reabsorption of phosphate remains virtually complete, even when filtered loads are reached which result in a substantial phosphaturia when phosphate has been administered. By comparing phosphate reabsorption and excretion in fasted animals, and in animals at various intervals after feeding, the existence of homeostatic adjustments in the renal tubular transport of inorganic phosphate has been demonstrated. The available evidence suggests that the intracellular disposition of phosphate itself may be an important factor in determining the rate of renal tubular phosphate transport at filtered loads in the physiological range. The limitations of the determination of the phosphate "Tm" as a device for studying homeostatic processes have been discussed.


Physiology ◽  
1986 ◽  
Vol 1 (3) ◽  
pp. 100-103 ◽  
Author(s):  
PC Brazy ◽  
LJ Mandel

Cells require inorganic phosphate for formation of ATP and a variety of other metabolic and transport functions. Studies of renal tubules indicate that availability of phosphate does regulate rates of oxidative metabolism and solute transport, that intracellular metabolic processes compete for inorganic phosphate, and that transepithelial phosphate transport provides inorganic phosphate for use within the cell.


1955 ◽  
Vol 33 (4) ◽  
pp. 638-650 ◽  
Author(s):  
James G. Foulks

By means of the infusion of small amounts of sodium sulphate it has been possible to elevate the filtered load of inorganic phosphate to the renal tubule in fasted dogs without the administration of exogenous phosphate. Under these circumstances, the reabsorption of phosphate remains virtually complete, even when filtered loads are reached which result in a substantial phosphaturia when phosphate has been administered. By comparing phosphate reabsorption and excretion in fasted animals, and in animals at various intervals after feeding, the existence of homeostatic adjustments in the renal tubular transport of inorganic phosphate has been demonstrated. The available evidence suggests that the intracellular disposition of phosphate itself may be an important factor in determining the rate of renal tubular phosphate transport at filtered loads in the physiological range. The limitations of the determination of the phosphate "Tm" as a device for studying homeostatic processes have been discussed.


1996 ◽  
Vol 251 (5) ◽  
pp. 580 ◽  
Author(s):  
Chulee Yompakdee ◽  
Nobuo Ogawa ◽  
Satoshi Harashima ◽  
Y. Oshima

Physiology ◽  
1987 ◽  
Vol 2 (2) ◽  
pp. 45-48
Author(s):  
H Murer ◽  
M Kerstin

Transcellular transport of inorganic phosphate (Pi) in the renal proximal tubule is sodium dependent. The entry step across the apical membrane involves a Na-Pi cotransport system and is subject to short-term and long-term regulation. This regulation can be protein synthesis independent (short term) as well as protein synthesis dependent (long term).


Sign in / Sign up

Export Citation Format

Share Document