Calcitonin decreases the renal tubular capacity for phosphate reabsorption

1983 ◽  
Vol 245 (3) ◽  
pp. F345-F348 ◽  
Author(s):  
R. K. Zalups ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Salmon Calcitonin ◽  
Phosphate Reabsorption ◽  
Pi Transport ◽  
Significant Difference ◽  
Presence And Absence ◽  
Renal Tubular ◽  
Synthetic Salmon Calcitonin

The effects of pharmacologic doses of synthetic salmon calcitonin on the renal tubular capacity of phosphate (Pi) transport were determined in the presence and absence of maximally phosphaturic doses of parathyroid hormone (PTH). Thyroparathyroidectomized rats were given graded infusions of Pi (1, 2, and 3 mumol/min) to prevent the hypophosphatemic effects of calcitonin and to determine the maximum transport of Pi for the kidney (TmPi/GFR). The maximum transport of Pi for the rats treated with calcitonin was 2.46 +/- 0.27 mumol/ml. This value was significantly less than that of 3.88 +/- 0.32 mumol/ml (P less than 0.05) for the control animals but was significantly greater than the maximum transport of Pi of 1.16 +/- 0.05 mumol/ml (P less than 0.05) for the rats treated with PTH. Furthermore, there was no significant difference between the maximum transport of Pi for the rats treated with PTH and that of 1.04 +/- 0.05 mumol/ml for the rats treated with PTH plus calcitonin. We conclude that pharmacologic doses of calcitonin decrease the tubular capacity for Pi reabsorption of the kidney and that the effect is significantly smaller than that of maximally phosphaturic doses of PTH.

Resistance to the phosphaturic effect of parathyroid hormone in the hamster

1979 ◽  
Vol 237 (3) ◽  
pp. F175-F181
Author(s):  
C. A. Harris ◽  
J. F. Seely
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Free Access ◽  
Calcium Excretion ◽  
Renal Tubular Cell ◽  
Acid Base ◽  
Significant Difference ◽  
Renal Tubular ◽  
Fractional Excretion Of Phosphate ◽  
Access To Food

The renal effects of parathyroid hormone (PTH) and dibutyryl 3'5'-cyclic AMP (DBcAMP) were studied in thyroparathyroidectomized hamsters. The hamsters were permitted free access to food and water or fasted for 16 h. PTH caused a phosphaturia in the fed hamster (fractional excretion of phosphate (FEPO4) increased from 5.8 +/- 1.3 to 27.4 +/- 4.6%, P less than 0.001) but not in the fasted hamster (from 9.9 +/- 2.5 to 12.4 +/- 2.5%, NS), whereas calcium excretion decreased significantly in both groups. There was no significant difference in blood acid-base or phosphate levels between the two groups. Insulin did not restore the phosphaturic response to PTH (FEPO4 from 7.7 +/- 2.6 to 5.3 +/- 1.7%), whereas phosphate or NH4Cl infusion did, FEPO4 increasing from 20.9 +/- 3.1 to 38.1 +/- 5.4% (P less than 0.02) and from 19.5 +/- 3.8 to 39.0 +/- 7.5%, respectively. DBcAMP caused a phosphaturia both in the fasted (from 9.6 +/- 2.7 to 20.1 +/- 4.5%, P less than 0.01) and fed (from 2.5 +/- 0.5 to 10.7 +/- 1.5%, P less than 0.02) hamster. A fasting state of up to 64 h did not produce resistance to PTH in the rat. It is concluded that fasting produces resistance to the phosphaturic but not the calcium-retaining effects of PTH in the hamster. The resistance may occur, at least partly, prior to the production of cAMP within the renal tubular cell.

scholarly journals Calcitonin-sensitive adenylate cyclase in rat renal tubular membranes

1975 ◽  
Vol 150 (3) ◽  
pp. 305-314 ◽  
Author(s):  
N Loreau ◽  
C Lepreux ◽  
R Ardaillou
Keyword(s):  
Parathyroid Hormone ◽  
Adenylate Cyclase ◽  
Salmon Calcitonin ◽  
Maximum Velocity ◽  
Membrane Receptors ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Human Calcitonin ◽  
Renal Tubular ◽  
Tubular Membranes

1. Renal tubular membranes from rat kidneys were prepared, and adenylate cyclase activity was measured under basal conditions, after stimulation by NaF or salmon calcitonin. Apparent Km value of the enzyme for hormone-linked receptor was close to 1 × 10(-8) M. 2. The system was sensitive to temperature and pH. pH was found to act both on affinity for salmon calcitonin-linked receptor and maximum stimulation, suggesting an effect of pH on hormone-receptor binding and on a subsequent step. 3. KCl was without effect areas whereas CoCl and CaCl2 above 100 muM and MnCl2 above 1 muM inhibited F--and salmon calcitonin-sensitive adenylate cyclase activities. The Ca2+ inhibition of the response reflected a fall in maximum stimulation and not a loss of affinity of salmon calcitonin-linked receptor for the enzyme. 4. The measurement of salmon calcitonin-sensitive adenylate cyclase activity as a function of ATP concentration showed that the hormone increases the maximum velocity of the adenylate cyclase. GTP, ITP and XTP at 200 muM did not modify basal, salmon calcitonin- and parathyroid hormone-sensitive adenylate cyclase activities. 5. Basal, salmon calcitonin- and F--sensitive adenylate cyclase activities decreased at Mg2+ concentrations below 10 mM. High concentrations of Mg2+ (100 mM) led to an inhibition of the F--stimulated enzyme. 6. Salmon calcitonin-linked receptor had a greater affinity for adenylate cyclase than human or porcine calcitonin-linked receptors. There was no additive effect of these three calcitonin peptides whereas parathyroid hormone added to salmon calcitonin increased adenylate cyclase activity, thus showing that both hormones bound to different membrane receptors. Human calcitonin fragments had no effect on adenylate cyclase activity. 7. Salmon calcitonin-stimulated adenylate cyclase activity decreased with the preincubation time. This was due to progressive degradation of the hormone and not to the rate of binding to membrane receptors.

Synthetic atrial natriuretic factor decreases renal tubular phosphate reabsorption in rats

1985 ◽  
Vol 249 (2) ◽  
pp. F315-F318
Author(s):  
T. G. Hammond ◽  
A. Haramati ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Atrial Natriuretic Factor ◽  
Tubular Reabsorption ◽  
Phosphate Reabsorption ◽  
Natriuretic Factor ◽  
Tubular Phosphate Reabsorption ◽  
Renal Tubular ◽  
Filtered Load ◽  
Atrial Natriuretic

Atrial natriuretic factor (ANF), a family of peptides isolated from cardiac atria, has marked effects on sodium excretion. A synthetic 26 amino acid sequence of ANF peptide has also been shown to be phosphaturic. However, it is difficult to assess whether the phosphaturia is due to changes in tubular reabsorption of phosphate without control of filtered load of phosphate. In the present study, the hypothesis that ANF peptide decreases tubular phosphate reabsorption was tested by using graded phosphate infusions of 0, 1, 2, and 3 mumol/min in thyroparathyroidectomized rats. Further, reabsorbed phosphate was similarly assessed in rats infused with parathyroid hormone (PTH) to allow comparison with a known phosphaturic hormone. ANF peptide decreased reabsorbed phosphate compared with saline controls (2.72 +/- 0.28 mumol/ml GFR compared with 3.35 +/- 0.35, P less than 0.05) but not as much as a maximally phosphaturic dose of PTH (2.04 +/- 0.13 mumol/ml GFR). We conclude that synthetic ANF peptide decreases tubular phosphate reabsorption in vivo.

Control of Renal Tubular Phosphate Reabsorption by Parathyroid Hormone in Man

1977 ◽  
Vol 53 (5) ◽  
pp. 431-438
Author(s):  
D. A. Walker ◽  
S. Joyce Davies ◽  
K. Siddle ◽  
J. S. Woodhead
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Primary Hyperparathyroidism ◽  
Normal Subjects ◽  
Vitamin D Metabolism ◽  
Phosphate Reabsorption ◽  
Important Regulator ◽  
Urinary Cyclic Amp ◽  
Renal Tubular

1. The maximum tubular reabsorption capacity for phosphate relative to glomerular filtration rate (Tm,P/GFR) was found to range from 0·8 to 1·5 mmol/l in 32 normal fasting subjects. In 14 patients with primary hyperparathyroidism and five patients with hyperparathyroidism secondary to vitamin D deficiency or malabsorption values ranged from 0·2 to 0·8 mmol/l. 2. Plasma parathyroid hormone concentrations measured by an immunoradiometric technique ranged from <0·15 to 0·9 ng/ml in the normal subjects and from 0·5 to 10 ng/ml in the patients with hyperparathyroidism. There was no correlation, however, between plasma parathyroid hormone and Tm,P/GFR in either normal or abnormal groups. 3. Plasma parathyroid hormone was lower in 11 out of 13 patients with primary hyperparathyroidism 3 or 4 weeks after tumour removal than immediately before the operation. In all cases there was a rise in Tm,P/GFR, though not all values were normalized. 4. Changes in plasma parathyroid hormone, Tm,P/GFR and plasma and urinary cyclic AMP concentrations were measured during infusion of bovine parathyroid hormone into normal fasting subjects. Phosphate reabsorption fell markedly in response to low doses of parathyroid hormone (0·5 i.u. h−1 kg−1), higher doses (4 i.u. h−1 kg−1) producing little additional change in Tm,P/GFR despite large changes in cyclic AMP excretion. At the highest doses used (8 i.u. h−1 kg−1) apparent saturation of the renal adenylate cyclase occurred. During an infusion of hormone, 0·25 i.u. h−1 kg−1 over 3 h, a fall in Tm,P/GFR was recorded at concentrations of immunoreactive parathyroid hormone within the normal range for endogeneous hormone. At such concentrations it was not possible to detect significant changes in either plasma or urine cyclic AMP. 5. It is concluded that parathyroid hormone is an important regulator of renal phosphate handling under normal physiological conditions. Such a regulatory process has been implicated in the control of vitamin D metabolism.

RENAL TUBULAR LOCALIZATION OF PARATHYROID HORMONE INDUCED URINARY CYCLIC ADENOSINE 3′,5′-MONOPHOSPHATE

1974 ◽  
Vol 77 (2) ◽  
pp. 282-286 ◽  
Author(s):  
Murphy T. Scurry ◽  
George L. Pauk
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Phosphorus Concentration ◽  
Phosphate Reabsorption ◽  
Before And After ◽  
Proximal Tubular ◽  
Urinary Cyclic Amp ◽  
Renal Tubular ◽  
Stop Flow

ABSTRACT Stop-flow studies were done in three dogs before and after a parathyroid hormone (PTH) infusion. The urine cyclic adenosine 3′,5′-monophosphate (cyclic AMP) to inulin U/P ratios did not change during the control stop-flow but with PTH rose sharply and significantly in the proximal tubular samples. The rise in cyclic AMP to inulin U/P ratios was correlated with the fall in phosphorus concentration in the same samples. The PTH induced urinary cyclic AMP enters the tubular fluid in the same proximal area of the tubule in which PTH is known to affect phosphate reabsorption.

scholarly journals P114 Effect of vitamin D on parathyroid hormone, serum calcium and bone mineral density in patients with primary hyperparathyroidism being managed conservatively

Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Mahrukh Khalid ◽  
Vismay Deshani ◽  
Khalid Jadoon
Keyword(s):  
Bone Mineral Density ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Bone Mineral ◽  
Serum Calcium ◽  
Mineral Density ◽  
Neck Of Femur ◽  
Vitamin D Levels ◽  
Significant Difference

Abstract Background/Aims  Vitamin D deficiency is associated with more severe presentation of primary hyperparathyroidism (PTHP) with high parathyroid hormone (PTH) levels and reduced bone mineral density (BMD). We analyzed data to determine if vitamin D levels had any impact on PTH, serum calcium and BMD at diagnosis and 3 years, in patients being managed conservatively. Methods  Retrospective analysis of patients presenting with PHPT. Based on vitamin D level at diagnosis, patients were divided into two groups; vitamin D sufficient (≥ 50 nmol/L) and vitamin D insufficient (≤ 50 nmol/L). The two groups were compared for age, serum calcium and PTH levels at diagnosis and after mean follow up of 3 years. BMD at forearm and neck of femur (NOF) was only analyzed in the two groups at diagnosis, due to lack of 3 year’s data. Results  There were a total of 93 patients, 17 males, mean age 70; range 38-90. Mean vitamin D level was 73.39 nmol/L in sufficient group (n = 42) and 34.48 nmol/L in insufficient group (n = 40), (difference between means -38.91, 95% confidence interval -45.49 to -32.33, p &lt; 0.0001). There was no significant difference in age, serum calcium and PTH at the time of diagnosis. After three years, there was no significant difference in vitamin D levels between the two groups (mean vitamin D 72.17 nmol/L in sufficient group and 61.48 nmol/L in insufficient group). Despite rise in vitamin D level in insufficient group, no significant change was observed in this group in PTH and serum calcium levels. BMD was lower at both sites in vitamin D sufficient group and difference was statistically significant at NOF. Data were analyzed using unpaired t test and presented as mean ± SEM. Conclusion  50% of patients presenting with PHPT were vitamin D insufficient at diagnosis. Vitamin D was adequately replaced so that at 3 years there was no significant difference in vitamin D status in the two groups. Serum calcium and PTH were no different in the two groups at diagnosis and at three years, despite rise in vitamin D levels in the insufficient group. Interestingly, BMD was lower at forearm and neck of femur in those with sufficient vitamin D levels and the difference was statistically significant at neck of femur. Our data show that vitamin D insufficiency does not have any significant impact on PTH and calcium levels and that vitamin D replacement is safe in PHPT and does not impact serum calcium and PTH levels in the short term. Lower BMD in those with adequate vitamin D levels is difficult to explain and needs further research. Disclosure  M. Khalid: None. V. Deshani: None. K. Jadoon: None.

Sign in / Sign up

Export Citation Format

Share Document