Secretion of Inorganic Phosphate in the Rat Nephron

1975 ◽  
Vol 48 (6) ◽  
pp. 475-489 ◽  
Author(s):  
J.-F. Boudry ◽  
U. Troehler ◽  
M. Touabi ◽  
H. Fleisch ◽  
J.-P. Bonjour
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Inorganic Phosphate ◽  
Specific Radioactivity ◽  
Distal Tubule ◽  
High Plasma ◽  
Tubular Secretion ◽  
Tubular Reabsorption ◽  
Anaesthetized Rats ◽  
Terminal Nephron

1. The existence of tubular secretion of inorganic phosphate (Pi) in the mammalian kidney has been investigated by studying the renal response of rats infused with sodium phosphate by three different techniques. 2. Clearance studies indicate that, in anaesthetized rats, the net tubular reabsorption decreases markedly in response to Pi infusion. In conscious rats, the clearance of Pi slightly exceeded that of inulin at high plasma Pi concentration. 3. Free-flow micropuncture in control rats showed a net tubular reabsorption of Pi along the proximal tubule, and probably between the end of the distal tubule and the ureteral urine. In phosphate-loaded rats, whether receiving parathyroid hormone or not, an apparent net secretion of Pi was observed between the end of the distal tubule and the ureteral urine. In the phosphate-loaded group receiving parathyroid hormone, net secretion was also observed very early in the proximal tubule followed by a predominant reabsorption along this segment. Thus the early proximal tubule and probably also the terminal nephron can be the site of either net reabsorption or net secretion. 4. Microperfusions of proximal tubules show a fall in the specific radioactivity of the perfused radioactive Pi solution, indicating entry of Pi into the lumen.

Tubular Handling of Phosphate along the Nephron of Thyroparathyroidectomized Rats Injected with Ethane-1-Hydroxy-1,1-Diphosphonate

1981 ◽  
Vol 60 (2) ◽  
pp. 171-177 ◽  
Author(s):  
R. C. Mühlbauer ◽  
J.-P. Bonjour ◽  
H. Fleisch
Keyword(s):  
Proximal Tubule ◽  
Bone Mineral ◽  
Adaptive Response ◽  
Distal Tubule ◽  
Tubular Reabsorption ◽  
Free Flow ◽  
Induced Changes ◽  
Terminal Nephron ◽  
Early Proximal Tubule

1. Previous studies have shown that in thyroparathyroidectomized rats injection of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) at doses that inhibit bone mineral retention (0.16 mmol = 10 mg of phosphorus/kg body wt. per day subcutaneously) leads to a decrease in the net tubular reabsorption of phosphate. 2. In the present work the tubular response to EHDP (0.16 mmol/kg body wt.) injected subcutaneously for 9 days has been localized by free-flow micropuncture in thyroparathyroidectomized rats. 3. The results show that the net tubular reabsorption of phosphate along the first portion of the (early) proximal tubule was markedly depressed in the EHDP-injected thyroparathyroidectomized rats compared with that in the pair-fed thyroparathyroidectomized control animals. In this latter group the delivery of phosphate to the distal tubule was larger than in the final urine, confirming previous reports. In the EHDP-injected thyroparathyroidectomized rats no difference in delivery of phosphate was found between the distal tubule and the final urine, suggesting that diphosphonate inhibited net reabsorption of phosphate in the terminal nephron. 4. The sites of the EHDP-induced changes in the tubular handling of phosphate were similar to those previously determined for the adaptive response to an increase in the supply of phosphate.

Posttranscriptional regulation of the proximal tubule NaPi-II transporter in response to PTH and dietary Pi

1999 ◽  
Vol 277 (5) ◽  
pp. F676-F684 ◽  
Author(s):  
Heini Murer ◽  
Ian Forster ◽  
Nati Hernando ◽  
Georg Lambert ◽  
Martin Traebert ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Posttranscriptional Regulation ◽  
Apical Membrane ◽  
Tubular Reabsorption ◽  
Transport Capacity ◽  
Phosphate Intake ◽  
Proximal Tubular ◽  
Dietary Phosphate ◽  
Proximal Tubular Reabsorption

The rate of proximal tubular reabsorption of phosphate (Pi) is a major determinant of Pi homeostasis. Deviations of the extracellular concentration of Piare corrected by many factors that control the activity of Na-Pi cotransport across the apical membrane. In this review, we describe the regulation of proximal tubule Pi reabsorption via one particular Na-Pi cotransporter (the type IIa cotransporter) by parathyroid hormone (PTH) and dietary phosphate intake. Available data indicate that both factors determine the net amount of type IIa protein residing in the apical membrane. The resulting change in transport capacity is a function of both the rate of cotransporter insertion and internalization. The latter process is most likely regulated by PTH and dietary Pi and is considered irreversible since internalized type IIa Na-Picotransporters are subsequently routed to the lysosomes for degradation.

Nephron heterogeneity of phosphate reabsorption: effect of parathyroid hormone

1984 ◽  
Vol 246 (2) ◽  
pp. F155-F158
Author(s):  
A. Haramati ◽  
J. A. Haas ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Loop Of Henle ◽  
Phosphate Reabsorption ◽  
Phosphate Excretion ◽  
Before And After ◽  
Superficial And Deep Nephrons ◽  
Nephron Heterogeneity

We evaluated the response of superficial and deep nephron proximal tubules to PTH in thyroparathyroidectomized (TPTX) rats fed a normal phosphate diet (0.7%). As phosphate reabsorption is not detectable in the ascending limb of the loop of Henle, fractional phosphate delivery (FDPi%) to the superficial early distal tubule and papillary loop of Henle reflects delivery from superficial and deep nephron proximal tubules, respectively. Re-collection micropuncture experiments were performed in nine acutely TPTX rats before and after the infusion of PTH (33 U/kg bolus; 1 U X kg-1 X min-1). In response to PTH, fractional phosphate excretion increased from 3.3 to 26.2% (P less than 0.05). FDPi% was less from the deep than from the superficial proximal tubule (5.7 vs. 15.7%, P less than 0.05) prior to PTH, indicating enhanced phosphate reabsorption by deep compared with superficial proximal tubules. During PTH infusion, FDPi% was increased in both nephron groups compared with control (P less than 0.05), but there were no differences in phosphate delivery between deep (28.0%) and superficial (29.7%) proximal tubules. We conclude that in acutely volume-expanded TPTX rats, infusion of a pharmacologic dose of PTH decreases phosphate reabsorption in both superficial and deep nephrons. Furthermore, the heterogeneity of FDPi% from deep compared with superficial proximal tubules seen in TPTX rats is absent during PTH infusion.

scholarly journals Effect of propranolol on phosphate reabsorption by superficial nephron segments in response to parathyroid hormone in phosphate-deprived rats.

1990 ◽  
Vol 1 (2) ◽  
pp. 200-204
Author(s):  
A Rybczynska ◽  
A Hoppe ◽  
F G Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Free Flow ◽  
Phosphate Deprivation ◽  
Phosphate Reabsorption ◽  
Nephron Segments ◽  
Pars Recta

Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone. The decreased phosphaturic response to parathyroid hormone in rats fed a low phosphate diet for 1 day can be restored by propranolol infusion. Free-flow micropuncture studies were performed to localize the nephron site of restoration of the phosphaturic effect of parathyroid hormone by propranolol in rats deprived of phosphate for one day. In animals fed low phosphate diet and in the presence of parathyroid hormone, propranolol infusion did not change phosphate delivery to the late proximal tubule; however, fractional delivery of phosphate to the early distal tubule was significantly increased from 18.3 +/- 2.9 to 32.2 +/- 4.1%. In rats fed a normal phosphate diet, propranolol infusion did not change phosphate delivery along the nephron. We conclude that the restoration of the phosphaturic effect of parathyroid hormone by propranolol infusion in rats deprived of phosphate for 1 day is primarily due to decreased reabsorption of phosphate by superficial loop segments, most likely the pars recta segment of the proximal tubule.

Tubular handling of Pi: localization of effects of 1,25(OH)2D3 and dietary Pi in TPTX rats

1981 ◽  
Vol 241 (2) ◽  
pp. F123-F128
Author(s):  
R. C. Muhlbauer ◽  
J. P. Bonjour ◽  
H. Fleisch
Keyword(s):  
Proximal Tubule ◽  
Inorganic Phosphate ◽  
Distal Tubule ◽  
Chronic Administration ◽  
Terminal Portion ◽  
Dihydroxyvitamin D3 ◽  
Reabsorptive Capacity ◽  
Clearance Studies ◽  
Early Portion ◽  
The Difference

Previous clearance studies have shown that chronic administration (26 pmol/day i.p. for 7 days) of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) decreases the tubular reabsorptive capacity for inorganic phosphate (Pi) in thyroparathyroidectomized (TPTX) rats. In the present study the tubular localization of this effect was examined by free-flow micropuncture in TPTX rats. At the mentioned dosage, 1,25(OH)2D3 inhibited net Pi reabsorption in the early portion of the proximal tubule. In addition, 1,25(OH)2D3 treatment altered the difference in Pi delivery between the distal tubule and the final urine, suggesting an inhibition of net Pi reabsorption along the terminal portion of the nephron, or, alternatively, admixture of tubular fluid with higher Pi concentration from deep nephrons. Finally, in TPTX rats the tubular localization of the effect of varying the dietary Pi content was found to be quite similar to that of 1,25(OH)2D3.

Effects of parathyroid hormone on electrolyte transport in the hamster nephron

1979 ◽  
Vol 236 (4) ◽  
pp. F342-F348 ◽  
Author(s):  
C. A. Harris ◽  
M. A. Burnatowska ◽  
J. F. Seely ◽  
R. A. Sutton ◽  
G. A. Quamme ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Electrolyte Transport ◽  
Puncture Site ◽  
Phosphate Reabsorption ◽  
Renal Electrolyte Transport ◽  
Clearance Studies ◽  
Calcium And Magnesium

Recollection micropuncture and clearance studies were carried out on thyroparathyroidectomized hamsters to clarify the localization of the effects of parathyroid hormone (PTH) on renal electrolyte transport. The clearance data confirmed that PTH inhibits phosphate and enhances calcium and magnesium reabsorption. These effects appeared to result from actions of the hormone in several parts of the nephron. In the proximal tubule PTH did not affect H2O reabsorption but inhibited phosphate reabsorption ((TF/P)PO4 increased from 0.46 +/- 0.04 to 0.57 +/- 0.03, P less than 0.02) and appeared to enhance calcium and magnesium reabsorption ((TF/UF)Ca decreased from 1.41 +/- 0.07 to 1.25 +/- 0.06, P less than 0.001, and (TF/UF)Mg from 1.66 +/- 0.10 to 1.51 +/- 0.08, P less than 0.05; in control animals (TF/UF)Ca increased from 1.51 +/- 0.10 to 1.65 +/- 0.11, P less than 0.01). PTH further inhibited phosphate reabsorption and enhanced calcium and magnesium reabsorption between the late proximal and early distal sites of puncture. Comparison of fractional deliveries of calcium and magnesium from the late distal tubule with their fractional excretions suggests an additional effect beyond the distal puncture site. The phosphaturic, but not the calcium- and magnesium-retaining, effects of PTH were abolished by a 16-h fast.

Nephron sites of action of nicotinamide on phosphate reabsorption

1984 ◽  
Vol 246 (1) ◽  
pp. F27-F31
Author(s):  
J. A. Haas ◽  
T. J. Berndt ◽  
A. Haramati ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Proximal Convoluted Tubule ◽  
Free Flow ◽  
Loop Of Henle ◽  
Phosphate Deprivation ◽  
Phosphate Reabsorption ◽  
Pars Recta ◽  
Sites Of Action

The administration of nicotinamide results in urinary phosphate excretions similar to those obtained with pharmacologic doses of parathyroid hormone (PTH). Free-flow micropuncture was performed to localize the nephron site(s) of inhibition of phosphate reabsorption by nicotinamide or PTH in thyroparathyroidectomized (TPTX) rats stabilized on a normal or low phosphate diet. In rats fed a normal phosphate diet phosphaturia was observed following either nicotinamide or PTH treatment. Nicotinamide inhibited phosphate reabsorption in the loop of Henle (pars recta) but not in the accessible proximal tubule. PTH inhibited phosphate reabsorption in both the accessible proximal tubule and the pars recta. In phosphate deprivation, the phosphaturic response to either nicotinamide or PTH was blunted. Although phosphate reabsorption was markedly inhibited in the accessible proximal tubule with both nicotinamide and PTH, subsequent reabsorption in the loop of Henle and distal tubule blunted the phosphaturia. We conclude that nicotinamide primarily inhibits phosphate reabsorption by the pars recta in rats fed a normal phosphate diet, whereas it inhibits phosphate reabsorption by the proximal convoluted tubule in rats fed a low phosphate diet. Furthermore, avid reabsorption of phosphate in the pars recta accounts for the resistance to the phosphaturic effect of nicotinamide or PTH seen in rats fed a low phosphate diet.

Effect of acute thyroparathyroidectomy on nephron acidification

1984 ◽  
Vol 246 (5) ◽  
pp. F569-F574 ◽  
Author(s):  
H. H. Bengele ◽  
E. R. McNamara ◽  
E. A. Alexander
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Acid Excretion ◽  
Acid Phosphate ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Net Acid Excretion

The effect of the absence of parathyroid hormone on nephron acidification was determined in rats after acute thyroparathyroidectomy (TPTX). Tubular fluid samples were obtained from the superficial late proximal tubule (LPT), the early distal tubule ( EDT ), and along the inner medullary collecting duct (IMCD), and the results were compared with those obtained from control rats. In the LPT after TPTX, pH was lower, 6.66 +/- 0.01 vs. 6.73 +/- 0.01, and ammonium and net acid delivery were increased significantly. In the EDT no differences in pH, bicarbonate, or net acid were found between groups, whereas ammonium and acid phosphate were significantly different. Along the IMCD in control rats, pH decreased from 6.58 to 5.21 and the addition of about 430 nmol/min of net acid was observed. After TPTX more net acid entered the duct and pH was lower, 5.66, but did not change; neither did the amount of bicarbonate, ammonium, acid phosphate, or net acid change significantly along the duct. Net acid excretion was not different, however, among groups. These results demonstrate that TPTX markedly affects nephron acidification, increasing net acid along the proximal tubule. In contrast to that in control rats, however, net acidification is completed prior to the IMCD. We conclude that the acute absence of parathyroid hormone may significantly affect local nephron acidification but does not alter acid excretion.

Renal tubular reabsorption of calcium and sodium in primary hyperparathyroidism

1990 ◽  
Vol 123 (2) ◽  
pp. 194-202 ◽  
Author(s):  
Jan H. Kristiansen ◽  
Jens Brøchner-Mortensen ◽  
Kaj O. Pedersen ◽  
Søren Jensen ◽  
Torben Glud
Keyword(s):  
Primary Hyperparathyroidism ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Tubular Reabsorption ◽  
Positive Linear Correlation ◽  
Calcium Reabsorption ◽  
Renal Tubular Reabsorption ◽  
The Absolute ◽  
Renal Tubular ◽  
Reabsorption Rate

Abstract. Nine patients with primary hyperparathyroidism were studied to investigate the renal tubular reabsorption of calcium and sodium. Fasting serum and urine samples were analysed, and the glomerular filtration rate and the renal plasma clearance of lithium were determined simultaneously. Comparison was made with 9 ageand sex-matched normocalcemic controls. In the proximal tubule, there was a significantly higher absolute reabsorption of calcium in patients than in controls, whereas the fractional reabsorption rate of calcium did not differ between the two groups. In the distal tubule, the absolute calcium reabsorption rate was significantly higher in the patients, whereas the fractional reabsorption rate of calcium was significantly lower than in controls. In the patient group there was a significantly positive linear correlation between the increased tubular capacity for calsium reabsorption and the absolute proximal calcium reabsorption rate, but not between the increased capacity and the absolute distal calcium reabsorption rate. No significant differences were found in the renal tubular handling of sodium between patients and controls. Our results suggest that the increased capacity for tubular calcium reabsorption in primary hyperparathyroidism mainly is localized in the proximal tubule, and that the renal tubular handling of calcium and sodium in this disease differs from that in familial hypocalciuric hypercalcemia.

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