scholarly journals Mode of action of parathyroid hormone and cyclic adenosine 3′,5′-monophosphate on renal tubular phosphate reabsorption in the dog

1971 ◽  
Vol 50 (3) ◽  
pp. 617-626 ◽  
Author(s):  
Zalman S. Agus ◽  
Jules B. Puschett ◽  
Dorothy Senesky ◽  
Martin Goldberg
Keyword(s):  
Parathyroid Hormone ◽  
Mode Of Action ◽  
Phosphate Reabsorption ◽  
Tubular Phosphate Reabsorption ◽  
Renal Tubular

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.

Effects of calcium on renal tubular phosphate reabsorption

1978 ◽  
Vol 234 (1) ◽  
pp. F22-F28 ◽  
Author(s):  
S. Goldfarb ◽  
M. Bosanac ◽  
M. Goldberg ◽  
Z. S. Agus
Keyword(s):  
Phosphate Reabsorption ◽  
Tubular Phosphate Reabsorption ◽  
Renal Tubular

scholarly journals OSR1-Sensitive Renal Tubular Phosphate Reabsorption

2012 ◽  
Vol 36 (1) ◽  
pp. 149-161 ◽  
Author(s):  
Ganesh Pathar ◽  
Michael Föller ◽  
Arezoo Daryadel ◽  
Kerim Mutig ◽  
Evgeny Bogatikov ◽  
...  
Keyword(s):  
Phosphate Reabsorption ◽  
Tubular Phosphate Reabsorption ◽  
Renal Tubular

Age, Renal Tubular Phosphate Reabsorption, and Serum Phosphate Levels in Adults

2008 ◽  
Vol 359 (8) ◽  
pp. 864-866 ◽  
Author(s):  
Massimo Cirillo ◽  
Carolina Ciacci ◽  
Natale G. De Santo
Keyword(s):  
Serum Phosphate ◽  
Phosphate Reabsorption ◽  
Tubular Phosphate Reabsorption ◽  
Renal Tubular

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.

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.

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