HOMEOSTATIC ADJUSTMENT IN THE RENAL TUBULAR TRANSPORT OF INORGANIC PHOSPHATE IN THE DOG

1955 ◽  
Vol 33 (4) ◽  
pp. 638-650 ◽  
Author(s):  
James G. Foulks
Keyword(s):  
Inorganic Phosphate ◽  
Renal Tubule ◽  
Phosphate Transport ◽  
Sodium Sulphate ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Transport Of Inorganic Phosphate ◽  
Renal Tubular ◽  
Filtered Load

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.

HOMEOSTATIC ADJUSTMENT IN THE RENAL TUBULAR TRANSPORT OF INORGANIC PHOSPHATE IN THE DOG

1955 ◽  
Vol 33 (1) ◽  
pp. 638-650 ◽  
Author(s):  
James G. Foulks
Keyword(s):  
Inorganic Phosphate ◽  
Renal Tubule ◽  
Phosphate Transport ◽  
Sodium Sulphate ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Transport Of Inorganic Phosphate ◽  
Renal Tubular ◽  
Filtered Load

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.

Alterations in renal tubular phosphate transport during intravenous infusion of parathyroid extract in the dog

1959 ◽  
Vol 196 (3) ◽  
pp. 567-571 ◽  
Author(s):  
James G. Foulks ◽  
Florence A. Perry
Keyword(s):  
Parathyroid Hormone ◽  
Intravenous Infusion ◽  
Phosphate Transport ◽  
High Threshold ◽  
Phosphate Excretion ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Parathyroid Extract ◽  
Renal Tubular ◽  
Adequate Rate

The intravenous infusion of parathyriod extract at an adequate rate (1–4 u/kg/hr.) invariably leads to phosphaturia which is primarily the result of altered renal tubular transport of the ion. In the intact fasted dog, several hours may be required for the infusion of parathyroid extract to reduce the initially high threshold for endogenous phosphate excretion below the filtered phosphate load. Other procedures which reduce the threshold for phosphate excretion may accelerate the onset of phosphaturia under these circumstances. However, the sluggish nature of this response suggests that parathyroid hormone does not contribute to the rapid adjustments in renal tubular phosphate transport which accelerate phosphate excretion following phosphate administration.

Renal tubular transport of water, solute, and PAH in rats loaded with isotonic saline

1965 ◽  
Vol 209 (6) ◽  
pp. 1199-1205 ◽  
Author(s):  
Marshall A. Cortney ◽  
Margaret Mylle ◽  
William E. Lassiter ◽  
Carl W. Gottschalk
Keyword(s):  
Proximal Tubule ◽  
Isotonic Saline ◽  
Urine Flow ◽  
Water Reabsorption ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Pah Clearance ◽  
Renal Tubular ◽  
Proximal Convolution ◽  
Filtered Load

Renal tubular transport of water, osmotically active solute, and PAH were studied with micropuncture methods in anesthetized rats loaded with a volume of 0.9% sodium chloride solution equivalent to 10% of their body weight. Inulin clearance and urine flow were greatly elevated above values in nondiuretic animals, but there was little change in PAH clearance. F/P inulin-C14OOH ratios indicated that 42% of the filtered water and solute was reabsorbed along the proximal convolution, a lower fraction than is found in nondiuretic and hypertonic saline-loaded rats. This indicates that the rate of solute and water reabsorption in the proximal tubule did not increase in proportion to the increased filtered load, and it was, in fact, similar to that in nondiuretic rats. Intravenous administration of vasopressin and aldosterone had no demonstrable effects on solute or water reabsorption. F/P PAH/inulin ratios demonstrated that PAH secretion occurred along the proximal tubule, but probably in no other portion of the nephron.

Renal Tubular Reabsorption of Acetoacetate, Inorganic Sulfate and Inorganic Phosphate in the Dog as Affected by Glucose and Phlorizin

1955 ◽  
Vol 184 (1) ◽  
pp. 91-96 ◽  
Author(s):  
Julius J. Cohen ◽  
Fredrik Berglund ◽  
William D. Lotspeich
Keyword(s):  
Inorganic Phosphate ◽  
Phosphate Transport ◽  
Tubular Reabsorption ◽  
Depressant Effect ◽  
Glucose Reabsorption ◽  
Tubular Transport ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Effect Of Glucose ◽  
Inorganic Sulfate

The effects of glucose and phlorizin on the maximal reabsorptive rates of acetoacetate, sulfate and phosphate were studied in the dog. Increased rates of glucose reabsorption depress maximal acetoacetate, sulfate and phosphate transport. Phlorizin not only reverses this depressant effect of glucose on these three ions, but actually raises their maximal reabsorptive rates above those of the control levels. These findings for acetoacetate and sulfate reabsorption are similar to those previously reported for phosphate reabsorption. The three ions, acetoacetate, sulfate and phosphate share a common reaction with glucose during their tubular transport. Glucose is the predominant compound, depressing any of the other three ions after they have reached maximal reabsorptive rates. The possible implications of these phenomena in the general problem of tubular transport are discussed.

AVP-stimulated nucleotide secretion in perfused mouse medullary thick ascending limb and cortical collecting duct

2009 ◽  
Vol 297 (2) ◽  
pp. F341-F349 ◽  
Author(s):  
Elvin Odgaard ◽  
Helle A. Praetorius ◽  
Jens Leipziger
Keyword(s):  
Collecting Duct ◽  
Tubular Secretion ◽  
Hormonal Control ◽  
Similar Response ◽  
Thick Ascending Limb ◽  
Cortical Collecting Duct ◽  
Medullary Thick Ascending Limb ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

Extracellular nucleotides are local, short-lived signaling molecules that inhibit renal tubular transport via both luminal and basolateral P2 receptors. Apparently, the renal epithelium itself is able to release nucleotides. The mechanism and circumstances under which nucleotide release is stimulated remain elusive. Here, we investigate the phenomenon of nucleotide secretion in intact, perfused mouse medullary thick ascending limb (mTAL) and cortical collecting duct (CCD). The nucleotide secretion was monitored by a biosensor adapted to register nucleotides in the tubular outflow. Intracellular Ca2+ concentration ([Ca2+]i) was measured simultaneously in the biosensor cells and the renal tubule with fluo 4. We were able to identify spontaneous tubular nucleotide secretion in resting perfused mTAL. In this preparation, 10 nM AVP and 1-desamino-8-d-arginine vasopressin (dDAVP) induced robust [Ca2+]i oscillations, whereas AVP in the CCD induced large, slow, and transient [Ca2+]i elevations. Importantly, we identify that AVP/dDAVP triggers tubular secretion of nucleotides in the mTAL. After addition of AVP/dDAVP, the biosensor registered bursts of nucleotides in the tubular perfusate, corresponding to a tubular nucleotide concentration of ∼0.2–0.3 μM. A very similar response was observed after AVP stimulation of CCDs. Thus AVP stimulated tubular secretion of nucleotides in a burst-like pattern with peak tubular nucleotide concentrations in the low-micromolar range. We speculate that local nucleotide signaling is an intrinsic feedback element of hormonal control of renal tubular transport.

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