scholarly journals Interrelations between phosphorus, calcium, parathyroid hormone, and renal phosphate excretion in response to an oral phosphorus load in normal and uremic dogs

1978 ◽  
Vol 14 (3) ◽  
pp. 207-214 ◽  
Author(s):  
Michael A. Kaplan ◽  
Janet M. Canterbury ◽  
George Gavellas ◽  
David Jaffe ◽  
Jacques J. Bourgoignie ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Phosphorus Load ◽  
Phosphate Excretion ◽  
Renal Phosphate Excretion

Phosphaturic effect of furosemide: role of PTH and carbonic anhydrase

1977 ◽  
Vol 232 (2) ◽  
pp. F105-F110 ◽  
Author(s):  
J. A. Haas ◽  
M. V. Larson ◽  
G. R. Marchand ◽  
F. C. Lang ◽  
R. F. Greger ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Carbonic Anhydrase ◽  
Extracellular Fluid ◽  
Constant Level ◽  
Extracellular Fluid Volume ◽  
Phosphate Excretion ◽  
Carbonic Anhydrase Inhibition ◽  
Renal Phosphate Excretion ◽  
Subsequent Administration

The first objective of this study was to examine the effects of furosemide on renal phosphate excretion in the presence and absence of a constant level of parathyroid hormone (PTH) while extracellular fluid volume was held constant. In the absence of PTH, furosemide did not significantly increase fractional phosphate excretion (FEP%, 4.2 +/- 2.7 to 6.2 +/- 1.9%; five dogs). In the presence of PTH, furosemide increased FEP% from 23.4 +/- 3.7 to 33.8 +/- 6.0% (P less .025; five dogs). Thus, the phosphaturia induced by furosemide was dependent on the presence of PTH. The second objective was to evaluate the hypothesis that furosemide exerts its phosphaturic effect through carbonic anhydrase inhibition, and therefore we tested for additivity of the phosphaturic effect of furosemide, and acetazolamide. In the presence of a constant level of PTH, acetazolamide increased FEP % from 24.5 +/- 1.8% to 40.7 +/- 5.1% P less than .025, five dogs. The subsequent administration of furosemide did not further increase FEP%, delta 3.3 +/- 8.9%; NS. Thus, the phosphaturic effect of furosemide was not additive to that of acetazolamide, indicating that acetazolamide and furosemide may share similar mechanisms for inhibiting phosphate reabsorption.

Effect of respiratory alkalosis on renal phosphate excretion

1982 ◽  
Vol 243 (5) ◽  
pp. F471-F475 ◽  
Author(s):  
A. Hoppe ◽  
M. Metler ◽  
T. J. Berndt ◽  
F. G. Knox ◽  
S. Angielski
Keyword(s):  
Parathyroid Hormone ◽  
Phosphate Uptake ◽  
Respiratory Alkalosis ◽  
Phosphate Transport ◽  
Phosphate Concentration ◽  
Dibutyryl Camp ◽  
Plasma Phosphate ◽  
Phosphate Reabsorption ◽  
Phosphate Excretion ◽  
Renal Phosphate Excretion

Respiratory alkalosis induced hypophosphatemia and hypophosphaturia in intact animals. The present studies evaluated the effect of respiratory alkalosis on tissue phosphate distribution and renal phosphate transport in the presence and absence of parathyroid hormone (PTH). Respiratory alkalosis decreased plasma phosphate concentration and increased phosphate concentrations in muscle and liver. It decreased fractional phosphate excretion (FEPi) from 6.1 +/- 1.4 to 0.6 +/- 0.2%. In thyroparathyroidectomized (TPTX) rats infused with 20 mM phosphate, respiratory alkalosis decreased FEPi from 15.0 +/- 0.9 to 5.5 +/- 0.1%. PTH or dibutyryl cAMP administration produced a phosphaturia that was blunted by respiratory alkalosis. The phosphaturic response to PTH was also blunted in hypocapnic rats in which alkalosis was prevented by infusion of HCl. We conclude that respiratory alkalosis increases phosphate uptake by muscle, which largely accounts for the hypophosphatemia. The kidney response with increased phosphate reabsorption independent of plasma and kidney phosphate concentrations and with refractoriness to the phosphaturic effect of PTH. This refractoriness to the phosphaturic effect of PTH is due to decreased PCO2 rather than to the concomitant extracellular alkalosis.

Effects of phosphate loading and parathyroid hormone on starling renal phosphate excretion

1980 ◽  
Vol 239 (3) ◽  
pp. F233-F243 ◽  
Author(s):  
R. F. Wideman ◽  
N. B. Clark ◽  
E. J. Braun
Keyword(s):  
Parathyroid Hormone ◽  
Phosphate Reabsorption ◽  
Phosphate Excretion ◽  
Wide Range ◽  
Tubular Phosphate Reabsorption ◽  
Tubular Transport ◽  
Phosphate Loading ◽  
Parathyroid Extract ◽  
Filtered Load ◽  
Renal Phosphate Excretion

The effects of phosphate loading were examined in intact, parathyroidectomized (PTX), and PTX starlings infused with parathyroid extract (PTX +/- PTE). In intact starlings, there was no correlation between the filtered phosphate load and the quantity of phosphate excreted. Net secretion predominated at lower filtered loads (2.5-20 mu mol . kg-1 . min-1) but net reabsorption occurred at filtered loads between 20 and 35 mu mol . kg-1 . min-1. Phosphate-loaded PTX starlings reabsorb phosphate over a wide range of filtered loads (5-45 mu mol . kg-1 . min-1). Excretion was significantly correlated with the filtered load in PTX birds (r = 0.943). Phosphate loaded PTX + PTE starlings secreted phosphate when filtered loads ranged from 2.5 to 30 mu mol . kg-1 . min-1. Excretion also was significantly correlated with the filtered load in this group (r = 0.972). The results of these experiments indicate that a) variations in endogenous PTH release in intact starlings result in wide variations in the renal pattern of phosphate excretion during phosphate loading; b) net phosphate secretion rarely occurs during phosphate loading in PTX starlings, but always occurs in PTX + PTE starlings; and c) both phosphate secretion and phosphate reabsorption are limited by maximal tubular transport capacities. Additional evidence indicates that PTH inhibits tubular phosphate reabsorption in starlings.

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.

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.

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.

Effect of cAMP analogue infusion on phosphate reabsorption in phosphate-deprived rats

1988 ◽  
Vol 255 (1) ◽  
pp. F96-F99
Author(s):  
T. J. Berndt ◽  
M. J. Onsgard ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Convoluted Tubule ◽  
Straight Tubule ◽  
Cyclic Monophosphate ◽  
Phosphate Reabsorption ◽  
Phosphate Excretion ◽  
Camp Analogue ◽  
Proximal Straight Tubule ◽  
Pars Recta ◽  
Distal Tubules

The present study was performed to compare the effects of 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate (cAMP analogue) and parathyroid hormone (PTH) infusion on segmental phosphate reabsorption in phosphate-deprived rats. Micropunctures of the late proximal and the early distal tubules were performed in acutely thyroparathyroidectomized (TPTX) rats fed either a normal (NPD) or low phosphate diet (LPD), and the phosphaturic response to infusion of PTH and cAMP analogue was evaluated. In NPD rats, PTH (n = 10) and the cAMP analogues (n = 11) markedly increased urinary phosphate excretion, due to inhibition of phosphate reabsorption along the proximal convoluted tubule and pars recta. In phosphate-deprived rats, PTH (n = 10) or the cAMP analogue (n = 11) did not increase urinary phosphate excretion. However, PTH and the cAMP analogue inhibited phosphate reabsorption along the proximal convoluted tubule but not in the pars recta in phosphate-deprived rats. We conclude that cAMP analogue infusion mimics the effect of PTH infusion on phosphate reabsorption along the proximal convoluted and proximal straight tubule in normal and phosphate-deprived rats. The resistance to the phosphaturic effect of PTH and cAMP infusions is a result of a blunted inhibition of phosphate reabsorption by the proximal convoluted tubule and also an increased phosphate reabsorption by the proximal straight tubule.

Phosphate excretion in uremic rats: effects of parathyroidectomy and phosphate restriction

1985 ◽  
Vol 248 (2) ◽  
pp. F175-F182
Author(s):  
E. Kraus ◽  
G. Briefel ◽  
L. Cheng ◽  
B. Sacktor ◽  
D. Spector
Keyword(s):  
Fractional Excretion ◽  
Tubular Reabsorption ◽  
Sprague Dawley ◽  
Dietary Regimen ◽  
Phosphate Excretion ◽  
Sprague Dawley Rats ◽  
Dietary Phosphate ◽  
Phosphate Loading ◽  
Fractional Excretion Of Phosphate ◽  
Renal Phosphate Excretion

As progressive renal failure develops, phosphate excretion per functioning nephron increases, thus preserving homeostasis. To test whether dietary phosphate supply might contribute to the regulation of renal phosphate excretion in the uremic setting, groups of male Sprague-Dawley rats that were either parathyroidectomized (PTX) or sham PTX (S-PTX) and either five-sixths nephrectomized (Nx) or sham Nx (S-Nx) were studied following a 4-wk dietary regimen consisting of 0.1 or 0.7% phosphate. For Nx rats fed the 0.7% phosphate diet the fractional excretion of phosphate (FEPi) was enhanced (47 +/- 6 vs. 21 +/- 3%) and the maximum tubular reabsorption of phosphate per milliliter GFR (TmPi/GFR) was suppressed (1.65 +/- 0.19 vs. 2.33 +/- 0.19 mumol/ml). FEPi was unchanged by PTX in these Nx animals (42 +/- 6 vs. 47 +/- 6%). TmPi/GFR remained suppressed in PTX, NX animals when compared with S-Nx, PTX controls (3.38 +/- 0.33 vs. 5.07 +/- 0.41 mumol/ml). For rats fed the 0.1% phosphate diet Nx did not affect TmPi/GFR in either S-PTX (5.40 +/- 0.43 vs. 4.97 +/- 0.34 mumol/ml) or PTX (7.03 +/- 0.23 vs. 6.98 +/- 0.21 mumol/ml) animals. For both S-Nx and Nx animals the effects of PTX and dietary phosphate restriction on TmPi/GFR were independent and additive. In all groups of animals, tubular reabsorption of phosphate per milliliter GFR (TRPi/GFR) dropped acutely with continued infusion of phosphate once TmPi/GFR was achieved. Thus, a resetting of TRPi/GFR occurs among Nx rats in response to both chronic dietary phosphate deprivation and acute intravenous phosphate loading.(ABSTRACT TRUNCATED AT 250 WORDS)

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