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.

NEWBORN URINARY CYCLIC AMP AND DEVELOPMENTAL RENAL RESPONSIVENESS TO PARATHYROID HORMONE

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 14-23 ◽  
Author(s):  
Louie G. Linarelli ◽  
John Bobik ◽  
Caroline Bobik
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenosine Monophosphate ◽  
Fourfold Increase ◽  
Before And After ◽  
Renal Action ◽  
Proximal Tubular ◽  
Insignificant Difference ◽  
Urinary Cyclic Amp ◽  
Renal Proximal Tubular

Since the renal action of parathyroid hormone is known to be mediated via 3',5'-adenosine monophosphate (cyclic AMP), urinary cyclic AMP studies were used to determine proximal tubular maturation. Ten formula fed full-term male infants showed a thirty- to sixtyfold increase in phosphate clearance and excretion with a three- to fourfold increase in urinary cyclic AMP comparing their first and third day 24-hour urines (2.37 ± 0.41 to 6.93 ± 0.96 Nm/mg creatinine M. ± S.E.M. first and third days respectively). Seven breast-fed infants showed cyclic AMP excretion of 3.6 ± 0.3 S.E.M. and 6.5 ± 0.3 S.E.M. on Day 1 and Day 3 respectively, showing an insignificant difference to the formula-fed infants. An additional 10 formula-fed infants 5 to 10 days of age excreted 7.0 ± 0.9 S.E.M. Nm/mg of creatinine which is comparable to the 3 to 4 days of age group. The threefold increase in cyclic AMP after the first day of life may possibly reflect increasing parathyroid renal responsiveness. One- and 3-day-old infants and adults were given a 1-hour parathyroid (PTH) infusion (5 U/kg/hr) with measurement of urinary cyclic AMP in time periods before and after the infusions. Peak increases in responses from baseline of cyclic AMP were 1.64 ± 0.34, 7.1 ± 1.5, and 36.0 ± 0.73 Nm/mg of creatinine M. ± range on first day, third day, and in adults respectively with similar relationships of increasing phosphate excretion. Thus, there is most likely a maturational renal proximal tubular responsiveness to PTH on the cellular cyclic AMP level.

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.

Impaired renal response to parathyroid hormone in potassium depletion

1975 ◽  
Vol 228 (1) ◽  
pp. 179-183 ◽  
Author(s):  
N Beck ◽  
BB Davis
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Renal Cortex ◽  
Rat Kidney ◽  
Potassium Depletion ◽  
Dibutyryl Cyclic Amp ◽  
Renal Response ◽  
Proximal Tubular ◽  
Urinary Cyclic Amp

In potassium depletion, a possible alteration of the proximal tubular response to parathyroid hormone (PTH) was evaluated in rat kidney. 1) There were impairments of both phosphaturic and urinary cyclic AMP responses to PTH. The site of the impairment was further investigated by studying the PTH-dependent cycle AMP system in renal cortex. 2) There was a lesser increase of cyclic AMP concentration by PTH in potassium-depleted slices, indicating the lesser urinary cyclic AMP was due to the specific impairment of PTH-dependent cyclic AMP in the kidney. 3). The activation of adenylate cyclase by PTH was impaired , but phosphodiesterase activity was not affected by potassium depletion, indicating the impairment of cyclic AMP generation was due to inhibition of adenylate cyclase. 4) The phosphaturic response to dibutyryl cyclic AMP infusion was also significantly less in the potassium-depleted animals, indicating the step subsquent to the cyclic AMP generation is also impaired. All above results indicate that, in potassium depletion, the renal response to PTH is impaired, and the impairment is both within the step of cyclic AMP generation and after the cyclic AMP generation.

scholarly journals Transcellular Diffusion of Non-Electrolytes across the Renal Tubular Epithelium

1962 ◽  
Vol 45 (4) ◽  
pp. 643-649 ◽  
Author(s):  
José Carlos Peña ◽  
Richard L. Malvin
Keyword(s):  
Tubular Epithelium ◽  
Permeability Characteristics ◽  
Molecular Weights ◽  
Renal Tubular Epithelium ◽  
Significant Movement ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Proximal Tubular Epithelium ◽  
Stop Flow ◽  
Transcellular Diffusion

The stop flow technique was used to investigate the permeability characteristics of the dog nephron to various C14-labeled non-electrolytes. 12 minutes after clamping the ureter, creatinine, PAH, and C14 compound were injected intravenously. 2 minutes later, urine samples were collected. Urea and glycerol were able to enter the tubular urine along the entire nephron at rates which were commensurate with their molecular weights. No significant movement of larger molecules (D-arabinose, D-glucose, and mannitol) could be detected. However, after administration of twenty units of pitressin, D-arabinose was able to diffuse across the distal and proximal tubular epithelium.

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.

Effect of parathyroid hormone on renal tubular permeability

1976 ◽  
Vol 231 (5) ◽  
pp. 1401-1407 ◽  
Author(s):  
WB Lorentz
Keyword(s):  
Parathyroid Hormone ◽  
Active Transport ◽  
Intravenous Infusion ◽  
Rat Kidney ◽  
Tubular Transport ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Tubular Permeability

The effect of parathyroid hormone (PTH) on renal tubular permeability has been studied utilizing micropuncture techniques in the rat kidney. After microinjection into superificial nephrons during control conditions, inulin (98.8 +/- 2.7%) and mannitol (97.2 +/- 2.4%) recovery from the experimental kidney was essentially complete. During intravenous infusion of PTH, inulin (99.3 +/- 2.9%) recovery was again complete. Mannitol recovery decreased signficantly after both early-proximal (84.7 +/- 5.8%, P less than 0.001) and late-proximal (89.7 +/- 2.8%, P less than 0.001) injections. There was no loss of either mannitol or inulin following distal tubular injection. Late-proximal TF/P inulin ratios during control conditions were 2.10 +/- 0.20 and decreased insignificantly to 1.99 +/- 0.21 during PTH infusion. Late-proximal TF/P mannitol rations were 2.09 +/- 0.21 during control periods and during PTH infusion decreased significantly to 1.78 +/- 0.19 (P less than 0.001). These results indicate that PTH induces a change in proximal tubular permeability to a usually impermeable nonelectrolyte, mannitol. The effects of PTH on proximal tubular transport could be partially explained by this alteration in permeability, which would increase passive backflux of actively transported species and decrease net transport while having no effect on active transport.

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.

Calcium-dependent, parathyroid hormone-independent regulation of 1,25-dihydroxyvitamin D

1980 ◽  
Vol 239 (2) ◽  
pp. E119-E124 ◽  
Author(s):  
U. Trechsel ◽  
J. A. Eisman ◽  
J. A. Fischer ◽  
J. P. Bonjour ◽  
H. Fleisch
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Calcium Intake ◽  
Dietary Calcium ◽  
Dihydroxyvitamin D ◽  
Calcium Dependent ◽  
1,25 Dihydroxyvitamin D ◽  
Urinary Cyclic Amp ◽  
Pth Level

The increase of plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) in response to Ca restriction has been suggested to be essentially mediated by parathyroid hormone (PTH). In this study, we have assessed the influence of variations in calcium intake on plasma 1,25(OH)2D in pair-fed sham-operated (sham) and in hypocalcemic hypoparathyroid rats after thyroparathyroidectomy (TPTX). In sham rats, plasma 1,25(OH)2D increased from 189 +/- 16 to 486 +/- 41 pM when dietary calcium was inreased from 1.2% Ca to 0.2% Ca. This increase was associated with an increase in plasma PTH level. In TPTX rats, plasma 1,25(OH)2D increased from 112 +/- 9 to 332 +/- 36 pM when dietary calcium was decreased. In this case, the increase was not associated with a rise in plasma PTH level nor with an increase in urinary cyclic AMP. When TPTX rats were infused chronically with PTH (60 U/day), plasma 1,25(OH)2D was 62 +/- 9 pM when the 1.2% Ca diet was given and 281 +/- 45 pM with the 0.2% Ca diet. These reults confirm that the thyroparathyroid glands influence plasma 1,25(OH)2D but they also provide evidence for a PTH-independent response of plasma 1,25(OH)2D to Ca restriction.

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