Renal tubular transport in phosphate depletion: a micropuncture study

1980 ◽  
Vol 58 (9) ◽  
pp. 1063-1071 ◽  
Author(s):  
Norman L. M. Wong ◽  
Gary A. Quamme ◽  
Thomas J. O'Callaghan ◽  
Roger A. L. Sutton ◽  
John H. Dirks

The acute effects of intravenous infusions of phosphate and parathyroid hormone (PTH) upon the renal tubular handling of sodium, potassium, calcium, magnesium, and phosphate were examined in phosphate-depleted dogs using recollection micropuncture techniques. Hypercalciuria in phosphate depletion results from an impairment of calcium reabsorption between proximal and distal sampling sites, which can be partially corrected by the acute administration of PTH or by phosphate infusion. Magnesium reabsorption was normal in phosphate-depleted dogs but increased in parallel with calcium in the distal tubule following PTH and phosphate infusion. Phosphate was avidly reabsorbed in the phosphate-depleted dog so that excretion was very low even during the infusion of PTH or of neutral phosphate. Only with the infusion of both PTH and phosphate was a normal phosphaturic response observed.

1964 ◽  
Vol 206 (6) ◽  
pp. 1355-1360 ◽  
Author(s):  
A. G. Ramsay

The stop-flow procedure was used to study the transport of H and K ions in the renal tubule during conditions of high and low pCO2. The increased rate of K excretion during respiratory alkalosis was due primarily to marked increase of K secretion at a distal site. The interrupted stop flow showed that K reabsorption was decreased at a site just proximal to the secretory area. This made a smaller contribution to the increased K excretion. The reciprocal relationship between tubular transport of K and H was demonstrable. CO2 tension appeared to influence HCO3 reabsorption and H secretion in both the distal and proximal tubule, whereas its effect on K transport was confined to the distal tubule. Hypercapnia never completely obliterated the distal secretory site. It is suggested that a pCO2-dependent H carrier is not shared with K. The increased K secretion of hypocapnia is more likely the result of increased K within the distal tubular cells.


1963 ◽  
Vol 205 (2) ◽  
pp. 281-285 ◽  
Author(s):  
P. Vishwakarma ◽  
T. Miller

The renal excretion of citrate and calcium was studied in the dog during the infusion of these substances alone or together by the stop-flow method. Citrate per se was found to be reabsorbed only in the proximal tubular area. This reabsorption occurred against marked concentration gradients. Spontaneous variations in the urine pH from 6.11 to 7.11 units did not affect the reabsorption in any way. Infusion of bicarbonate decreased the capacity of the proximal tubule to lower the citrate concentration but did not alter the general pattern of its transport along the nephron length. Calcium without citrate was actively reabsorbed only in the distal tubule. Calcium when given with citrate, did not affect the pattern of citrate transport along the length of the nephron. Citrate did not affect the distal reabsorption of calcium. However, it did produce a proximal reabsorption of calcium. It was postulated that the proximal reabsorption of citrate is active. The molecular requirement for reabsorption of citric acid is discussed.


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.


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