Parathyroid hormone-induced phosphate excretion following preequilibration with 32P

1984 ◽  
Vol 246 (4) ◽  
pp. F373-F378 ◽  
Author(s):  
R. F. Wideman
Keyword(s):  
Parathyroid Hormone ◽  
Inorganic Phosphate ◽  
Fractional Excretion ◽  
Secretory Component ◽  
Experimental Animals ◽  
Phosphate Excretion ◽  
Pi Transport

Parathyroid hormone (PTH) stimulates a secretory component of avian renal inorganic phosphate (Pi) transport, but the secreted Pi does not appear to be derived directly from peritubular (plasma) Pi. In the present study, experiments were conducted to determine whether differences in parathyroid status during 32P infusion influenced entry of the isotope into the Pi secretory pool. Fractional excretion values for Pi (FEPi) and 32P (FE32P) were compared in normal and parathyroidectomized (PTX) anesthetized birds that had been preinfused with 32P for 0, 90, and 240 min before PTH infusion. The results demonstrate that in the absence of exogenous PTH, FEPi is identical to FE32P in normal and PTX birds, reflecting full equilibration of 32P with excreted Pi under these conditions; and, regardless of the duration of 32P preequilibration or the parathyroid status of the experimental animals, exogenous PTH always causes FEPi to exceed FE32P. It is concluded that the Pi secretory pool is inaccessible to 32P under conditions that should markedly alter cellular Pi influx and efflux.

scholarly journals Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

2019 ◽  
Author(s):  
Forough Saki ◽  
Seyed Reza Kassaee ◽  
Azita Salehifar Salehifar ◽  
gholamhossein Ranjbar omrani
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Case Control Study ◽  
Fractional Excretion ◽  
Case Control ◽  
Control Group ◽  
Phosphate Excretion ◽  
Significant Difference ◽  
Fgf 23 ◽  
Control Study

Abstract Background:phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters II a and II c . However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods:In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results:The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P <0.001, r = 0.79). Conclusions:Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

Lithium administration and phosphate excretion

1976 ◽  
Vol 231 (4) ◽  
pp. 1140-1146 ◽  
Author(s):  
JA Arruda ◽  
JM Richardson ◽  
JA Wolfson ◽  
L Nascimento ◽  
DR Rademacher ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Renal Cortex ◽  
Cyclic Adenosine Monophosphate ◽  
Fractional Excretion ◽  
Adenosine Monophosphate ◽  
Adenyl Cyclase ◽  
Phosphate Excretion ◽  
Camp System

The phosphaturic effect of parathyroid hormone (PTH), cyclic adenosine monophosphate (cAMP), acetazolamide (Az), and HCO3 loading was studied in normal, thyroparathyroidectomized (TPTX), and Li-treated dogs. PTH administration to normal animals markedly increased fractional excretion (F) of PO4 but had a blunted effect on FPO4 in the Li-treated animals. Cyclic AMP likewise markedly increased FPO4 in the normal animals but had a markedly blunted effect in the Li-treated animals. Az led to a significant increase in FNa, FHCO3, and FPO4 in the normal animals. In the Li-treated dogs, Az induced a significant natriuresis and bicarbonaturia but failed to increase phosphaturia. HCO3 loading in normal dogs caused a significant phosphaturia while having little effect on FPO4 in Li-treated dogs. HCO3 loading to TPTX dogs was associated with a lower FPO4 as compared to normal HCO3-loaded animals. These data suggest that Li administration not only blocks the adenyl cyclase-cAMP system in the renal cortex, but it may also interfere with a step distal to the formation of cAMP, since the phosphaturic effect of both PTH and cAMP was markedly diminished in Li-treated animals.

Phosphaturic effect of L-NMMA in the presence of parathyroid hormone

1996 ◽  
Vol 271 (6) ◽  
pp. R1477-R1480
Author(s):  
M. J. Onsgard-Meyer ◽  
R. J. Kerrigan ◽  
M. Collins ◽  
A. A. Khraibi ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Parathyroid Glands ◽  
Constant Infusion ◽  
Sprague Dawley ◽  
Phosphate Excretion ◽  
Sprague Dawley Rats ◽  
Additional Group ◽  
Renal Clearances ◽  
Intact Rats

The objective of this study was to examine the effect of NG-monomethyl-L-arginine (L-NMMA) on phosphate excretion in the presence and absence of parathyroid hormone (PTH). Renal clearances were obtained before and during infusion of L-NMMA (15 mg/kg bolus and 500 micrograms.kg-1.min-1 infusion) in Sprague-Dawley rats with intact parathyroid glands (n = 6), in thyroparathyroidectomized (TPTX) rats receiving a constant infusion of PTH-(1-34) (0.01-0.03 U.kg-1.min-1) (n = 11) throughout the experiment, or in TPTX rats, that received an acute infusion of PTH-(1-34) (33 U/kg bolus and 1 U.kg-1.min-1 infusion) after L-NMMA infusion alone (n = 7). In rats with intact parathyroid glands, L-NMMA increased the fractional excretions of phosphate (FEPi) and sodium (FENa) and mean arterial pressure (MAP) (delta 8.6 +/- 1.5%, delta 0.62 +/- 0.1%, and delta 26.7 +/- 4.9 mmHg, respectively; P < 0.05). In TPTX rats receiving a constant infusion of PTH, L-NMMA again increased FEPi, FENa, and MAP (delta 9.5 +/- 3.6%, delta 1.1 +/- 0.4%, and delta 28.4 +/- 4.5 mmHg, respectively; P < 0.05). However, in TPTX rats, L-NMMA alone did not increase FEPi (delta 0.9 +/- 0.3%), whereas the subsequent infusion of PTH with L-NMMA increased FEPi (delta 15.6 +/- 3.1%; P < 0.05). In an additional group of intact and TPTX rats, the fractional excretion of lithium (FELi) was measured as an index of proximal reabsorption. L-NMMA increased FELi in intact rats (delta 13.2 +/- 2.6%; P < 0.05), but not in TPTX rats (delta 4.2 +/- 3.3%). In conclusion, L-NMMA increases phosphate excretion in association with increases in MAP and FENa, and this phosphaturic effect is dependent on the presence of PTH.

Effects of 1,25-dihydroxycholecalciferol on phosphate transport in vitamin D-deprived rats

1984 ◽  
Vol 247 (1) ◽  
pp. F177-F184 ◽  
Author(s):  
B. R. Kurnik ◽  
K. A. Hruska
Keyword(s):  
Vitamin D ◽  
Membrane Vesicles ◽  
Fractional Excretion ◽  
Phosphate Transport ◽  
Vitamin D Metabolites ◽  
Deficient Diet ◽  
Phosphate Excretion ◽  
Pi Transport ◽  
Undetectable Plasma ◽  
Proximal Tubular

To clarify the role of vitamin D in renal phosphate transport, weanling rats were fed a vitamin D-deficient diet containing 1.8% calcium and 1.2% phosphorus. After 5-6 wk, the rats were normocalcemic, normophosphatemic, and had normal levels of PTH. Assays of vitamin D metabolites revealed undetectable plasma levels of 25(OH)D, and 1,25(OH)2D levels of 92 +/- 16 pg/ml in partially vitamin D-depleted (PVDD) rats and 169 +/- 58 pg/ml in normal rats. PVDD rats had increased phosphate excretion, both absolute and fractional, and a decrease in Na+ gradient-dependent Pi transport in proximal tubular brush border membrane vesicles (BBMV) prepared from their kidneys. Vitamin D repletion of PVDD rats with 1,25(OH)2D3, 15 pmol/100 g body wt, decreased fractional excretion of Pi from 22.6 +/- 1.9 to 13.5 +/- 1.3%; the latter values were similar to normal rats. Repletion with 1,25(OH)2D3 also increased Na+-dependent phosphate transport in BBMV from 322 +/- 24 pmol X mg protein-1 X 15 s-1 in BBMV from PVDD rats to 698 +/- 70 pmol X mg protein-1 X 15 s-1. Repletion with larger doses of 1,25(OH)2D3 produced hypercalcemia and hyperphosphatemia from intestinal absorption, an increase in phosphate excretion, and a blunted response of Pi transport to 1,25(OH)2D3. Prevention of hyperphosphatemia by dietary adjustments allowed full expression of the stimulatory effects of 1,25(OH)2D3 on Pi transport. These later data may partially explain the inhibitory effects reported in prior studies in which plasma Pi was not controlled and the larger doses of 1,25(OH)2D3 administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Developmental changes in the phosphaturic response to parathyroid hormone in the rat

1985 ◽  
Vol 249 (2) ◽  
pp. F251-F255 ◽  
Author(s):  
S. K. Webster ◽  
A. Haramati
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Developmental Changes ◽  
High Dose ◽  
Kidney Weight ◽  
Phosphate Excretion ◽  
Immature Rats ◽  
Glomerular Filtrate ◽  
Old Rats ◽  
Fractional Excretion Of Phosphate

The need for young, immature rats to maintain positive phosphate balance for growth is well recognized. However, whether this process is associated with a resistance to the phosphaturic effect of parathyroid hormone (PTH) is not clear. In these experiments we examined the effect of PTH on urinary phosphate and cAMP excretion in rats at 3, 6, 12, and 20 wk of age. Clearance experiments were performed in acutely thyroparathyroidectomized (TPTX) rats fed a normal phosphate diet (0.86%). Basal fractional excretion of phosphate (FEPi) was low in all TPTX rats (less than 1%). The phosphaturic response to a high dose of PTH (1 U X kg-1 X min-1) increased with development (from 4 to 29%). The responses to increasing doses of PTH demonstrated a decrease in sensitivity to PTH in 6- compared with 20-wk-old rats. Urinary cAMP excretion (either per milliliter glomerular filtrate or per gram kidney weight) following PTH was not different among 6-, 12-, and 20-wk-old rats, thus demonstrating a dissociation between the increase in phosphate excretion and cAMP excretion. These results indicate that the phosphaturic response to PTH is blunted in immature, acutely TPTX rats and that the phosphaturia increases progressively with development.

THE EFFECT OF PARATHYROID HORMONE ON PHOSPHATE EXCRETION IN THE RAT

1953 ◽  
Vol 9 (3) ◽  
pp. 292-300 ◽  
Author(s):  
BERYL M. A. DAVIES ◽  
A. H. GORDON
Keyword(s):  
Parathyroid Hormone ◽  
Inorganic Phosphate ◽  
Phosphate Level ◽  
Aluminium Sulphate ◽  
Phosphate Excretion ◽  
Serum Inorganic Phosphate ◽  
Serum And Urine

The magnitude of the decrease in serum inorganic phosphate and the increase in urine phosphate of parathyroidectomized rats caused by injected parathyroid hormone has been studied. About 3 u.s.p. units of this hormone have been found to cause maximum changes in both serum and urine phosphate. Both responses depend on the respective initial phosphate level. Urine phosphate levels too high for more than minimal changes in phosphate excretion have been reduced by diets containing aluminium sulphate.

scholarly journals Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

2019 ◽  
Author(s):  
Forough Saki ◽  
Seyed Reza Kassaee ◽  
Azita Salehifar Salehifar ◽  
gholamhossein Ranjbar omrani
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Case Control Study ◽  
Fractional Excretion ◽  
Case Control ◽  
Control Group ◽  
Phosphate Excretion ◽  
Significant Difference ◽  
Fgf 23 ◽  
Control Study

Abstract Background phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters IIa and IIc. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal control population(P <0.001, r = 0.79). Conclusions Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

Regulation of Na-dependent Pi transport by parathyroid hormone in osteoblast-like cells

1989 ◽  
Vol 256 (1) ◽  
pp. E93-E100 ◽  
Author(s):  
T. Selz ◽  
J. Caverzasio ◽  
J. P. Bonjour
Keyword(s):  
Parathyroid Hormone ◽  
Cell Line ◽  
Inorganic Phosphate ◽  
Maximal Response ◽  
Pi Transport ◽  
Alanine Transport ◽  
Transport Of Inorganic Phosphate ◽  
Dependent Transport ◽  
Umr 106 ◽  
Stimulation Of

In the present work we investigated the influence of parathyroid hormone (PTH) on the transport of inorganic phosphate (Pi) in the osteoblast-like cell line UMR-106. Pi was transferred from the extra- to the intracellular compartment by means of a Na-dependent transport system with an apparent binding affinity for both Pi and Na similar to that recently observed in the osteoblast-like cell line ROS 17/2.8 (Calcif. Tissue Int. 43: 83-87, 1988). Exposure of confluent UMR-106 cells to PTH (10(-9)-10(-7) M) induced a concentration-related stimulation of the Na-dependent Pi transport (NaPiT). An increase in NaPiT was observed after a 1-h exposure to 10(-7) M PTH, with the maximal response occurring at 4-6 h. (PTH, 35.6 +/- 0.3; vehicle, 27.4 +/- 0.2 pmol.microgram DNA-1.4 min-1, P less than 0.001). The stimulatory effect of PTH on NaPiT was not associated with a change in the Na-dependent alanine transport. A positive correlation was observed between the increase of NaPiT and that of cAMP in response to various concentrations of PTH. Stimulation of cAMP by forskolin (10(-4) M) mimicked the effect of PTH on NaPiT. Kinetic analysis of the PTH-induced stimulation of NaPiT indicated an increase in Vmax (PTH, 226.9 +/- 6.9; vehicle, 182.9 +/- 1.9 pmol Pi/microgram DNA, P less than 0.001), with no change in Km. The increase in NaPiT by either PTH or forskolin was followed by a transient inhibition from 6 to 24 h that was associated with a decrease in the Na-dependent alanine transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Tubular localization of adaptation to dietary phosphate in rats

1977 ◽  
Vol 233 (4) ◽  
pp. F342-F348
Author(s):  
R. C. Muhlbauer ◽  
J. P. Bonjour ◽  
H. Fleisch
Keyword(s):  
Adaptive Response ◽  
Inorganic Phosphate ◽  
Renal Tubule ◽  
Distal Tubule ◽  
Fractional Excretion ◽  
Secretory Component ◽  
Transport Capacity ◽  
Terminal Part ◽  
Dietary Phosphate ◽  
The Difference

The renal tubule of rats adapts its transport capacity for inorganic phosphate (Pi) in response to changes in dietary Pi intake. Tubular localization of this adaptation was studied in rats pair-fed for 10 days a low (LPD), i.e., 0.2 g/100 g, or a high (HPD), i.e., 1.8 g/100 g, phosphorus diet. Free-flow micropunctures under acute Pi infusion were made at elevated but similar filtered loads of Pi: LPD, 6.07 +/- 0.29 (n, 32); HPD 5.34 +/- 0.24 (n, 33) micromol/kidney per min. Fractional excretion of Pi (FEPi) for the whole kidney was: LPD, 0.26 +/- 0.02 (n, 32); HPD, 0.67 +/- 0.02 (n, 33) (P less than 0.001). The fraction of filtered Pi found at various puncture sites suggests that part of the adaptation to dietary Pi occurs in the early proximal tubule. An effect in the later portion of the proximal convoluted tubule cannot be excluded in the present experiments. Furthermore, dietary Pi affects markedly the difference in Pi delivery between distal tubule and final urine. This could be due to a greater adaptive response of deep nephrons. Alternatively, the results could also indicate that an adaptation with a secretory component takes place along the terminal part of the nephrons.

Comparison of the effects of parathyroid hormone (PTH) and recombinant PTH-related protein on bicarbonate excretion by the isolated perfused rat kidney

1990 ◽  
Vol 126 (3) ◽  
pp. 403-408 ◽  
Author(s):  
A. G. Ellis ◽  
W. R. Adam ◽  
T. J. Martin
Keyword(s):  
Parathyroid Hormone ◽  
Rat Kidney ◽  
Urine Volume ◽  
Clinical Manifestations ◽  
Fractional Excretion ◽  
Bicarbonate Concentration ◽  
Isolated Perfused Rat Kidney ◽  
Amino Terminal ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney

ABSTRACT The isolated perfused rat kidney was used to study the effects of amino-terminal fragments of human parathyroid hormone, hPTH(1–34), bovine parathyroid hormone, bPTH(1–84) and of PTH-related proteins, PTHrP(1–34), PTHrP(1–84), PTHrP(1–108) and PTHrP(1–141) on urinary bicarbonate excretion. PTHrP(1–34) (7 nmol/l), bPTH(1–84) (5·5 nmol/l) and hPTH(1–34) (7 nmol/l) had similar effects in increasing bicarbonate excretion with respect to the control. At lower concentrations (0·7 nmol/l) all PTHrP components, but not hPTH(1–34) or bPTH(1–84) increased bicarbonate excretion significantly. Infusions of PTHrP(1–108) and PTHrP(1–141) at 0·7 nmol/l, while associated with a rise in urinary bicarbonate concentration and excretion during the early stages of perfusion, produced a sharp decline in bicarbonate concentration and excretion in the latter part of perfusion. The different peptides produced no significant differences in glomerular filtration rate, fractional excretion of sodium or urine volume. The absence of substantial differences between the effects of hPTH(1–34) and PTHrP(1–34) are as noted in previous studies. The differences between PTHrP(1–108)/PTHrP(1–141) and PTHrP(1–34) demonstrated here are consistent with (1) the clinical manifestations of acidosis in hyperparathyroidism and alkalosis in humoral hypercalcaemia of malignancy, and (2) an independent action of a component of PTHrP beyond amino acids 1–34. Journal of Endocrinology (1990) 126, 403–408

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