Phosphorus homeostasis in sheep. III.* Relationship between the amount of salivary phosphorus secreted and the quantities of phosphorus excreted via the urine and faeces

1974 ◽  
Vol 25 (3) ◽  
pp. 495 ◽  
Author(s):  
FM Tomas

The interrelationships between the urinary and faecal pathways for phosphorus excretion in sheep have been examined under conditions allowing direct proportional control of the major portion of endogenous phosphorus secretion to the gut which is contributed by the parotid salivary glands. Two rumen-fistulated Merino wethers were fitted with permanent bilateral re-entrant parotid duct cannulas which allowed continuous collection and return of parotid saliva. During experimental periods, a proportion of the phosphorus secreted by the parotid glands during control periods was returned to the rumen in artificial saliva, and the remaining quantity not returned in this manner was infused intravenously over a corresponding time period. Diversion of the secreted parotid salivary phosphorus from the rumen to the blood led to an increase in urinary phosphorus excretion which was proportional to the fractional amount of secreted phosphorus withheld from the rumen. Phosphorus balance remained unaltered, which indicated a virtual substitution between the two excretory pathways. The increased urinary excretion of phosphorus is attributed partly to increased plasma phosphorus levels and partly to a reduced efficiency of renal tubular reabsorption of phosphorus. No direct evidence for any hormonal action could be seen. The data show that the pathway of excretion of phosphorus can be determined quantitatively by the rate of endogenous phosphorus secretion into the gut. This mechanism is of fundamental importance among factors contributing to phosphorus homeostasis in sheep. ____________________ *Part II, Aust. J. Agric. Res., 25: 485 (1974).

1974 ◽  
Vol 25 (3) ◽  
pp. 475 ◽  
Author(s):  
FM Tomas ◽  
M Somers

The effects of bilateral parotid duct ligation upon calcium and phosphorus concentrations in blood plasma and upon phosphorus excretion in urine and faeces have been examined. Five Merino wethers were used, of which three were given a phosphorus-deficient diet (0.304 g phosphorus/day) and two a phosphorus-sufficient diet (1.454 g phosphorus/day) for 32 days prior to ligation of the parotid ducts. Blood samples were taken every 6 hours for 2 days before and 4 days after parotid duct ligation followed by less frequent sampling for a further 3 days. Parotid duct ligation caused an increase in plasma inorganic phosphorus levels after the first day in the phosphorus-supplemented sheep and in one of the deficient animals. Plasma calcium concentrations tended to be inversely related to plasma phosphorus levels and showed marked variations on the fourth day following duct ligation, coinciding with a sudden fall in plasma phosphorus levels of 30-50 %. Urinary phosphorus excretion in the phosphorus-sufficient animals was increased 20 to 50-fold following ligation and reached a peak of about 600 mg/day on the fourth day, but there was no significant change in phosphorus balance. Marked alterations in the daily urinary output of phosphorus tended to be associated with a change in plasma phosphorus levels in the reverse direction. Four of the sheep were re-examined 22 months after duct ligation and the elevated urinary output of phosphorus was found to have persisted in three of the four animals. It appears that there is a relationship between the salivary secretion of phosphorus to the gut and the urinary phosphorus excretion which contributes towards maintenance of the phosphorus homeostasis in sheep.


1974 ◽  
Vol 75 (1) ◽  
pp. 50-63 ◽  
Author(s):  
Kristian F. Hanssen

ABSTRACT Twenty newly diagnosed, but as yet untreated patients of both sexes with classical juvenile diabetes were investigated by determining the mean plasma immunoreactive growth hormone (IRHGH) and urinary IRHGH for a 24 hour period before and during initial insulin treatment. The plasma IRHGH was significantly higher (0.05 > P > 0.01) before than during initial insulin treatment. During initial insulin treatment, the mean plasma IRHGH was significantly higher (0.01 > P > 0.001) than in a control group. The urinary IRHGH was significantly higher (0.01 > P > 0.001) before than during insulin treatment. The increased urinary IRHGH observed before insulin treatment is thought to be partly due to a defective renal tubular reabsorption of growth hormone. No significant correlation was found between the mean blood sugar and plasma or urinary IRHGH either before or during insulin treatment.


2011 ◽  
Vol 164 (5) ◽  
pp. 839-847 ◽  
Author(s):  
Andrea Trombetti ◽  
Laura Richert ◽  
Karine Hadaya ◽  
Jean-Daniel Graf ◽  
François R Herrmann ◽  
...  

BackgroundWe examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism.MethodsWe measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10–13) after renal transplantation.ResultsHypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108–288) vs 48 (40–64) ng/l, P<0.002 for intFGF-23; 205 (116–384) vs 81 (55–124) U/ml, P<0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (r=−0.35, P<0.003; −0.35, P<0.003, respectively), and TmPi/GFR (r=−0.50, P<0.001; −0.54, P<0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pre-transplant levels of FGF-23 were not associated with sPi at the time of transplantation.ConclusionIn addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.


1965 ◽  
Vol 208 (6) ◽  
pp. 1165-1170 ◽  
Author(s):  
W. Joseph Rahill ◽  
Mackenzie Walser

Simultaneous clearances of inulin, calcium, and either Be7, Ba140, or Ra226, given by constant infusion, were measured in salt-depleted dogs or dogs undergoing mild saline, mannitol, or sulfate diuresis. Urine-to-plasma ratios of all three cations less than 0.5 were noted, suggesting that all can be actively reabsorbed. Clearances of barium and radium were correlated with calcium clearance, but the clearance of beryllium was unpredictable. Protein binding of beryllium was shown to be of the same order of magnitude as other alkaline earths when errors due to adsorption of Be7 onto containers were minimized. Protein binding of barium averaged 54%. The excreted-to-filtered ratio for barium was a constant power (.54) of the ratio for calcium. The data do not exclude the possibility that these cations are reabsorbed by a common transport mechanism with calcium.


10.3823/2537 ◽  
2017 ◽  
Vol 10 ◽  
Author(s):  
Humberto Ferreira Arquez

Background: The paired parotid glands are the largest of the major salivary glands and produces mainly serous secretions. The secretion of this gland reaches the oral cavity through single parotid duct (Stensen’s duct). The parotid duct begins at the anterior border of the gland, crosses the masseter muscle, and then pierces the buccinator muscle to reach the mucosa lining the mouth at the level of the cheek. The purpose of this study is determine the morphologic features of the parotid duct and describe an anatomical variation until now unreported. Methods and Findings: A total of 17 cadavers were used for this study in the Morphology Laboratory at the University of Pamplona. In a cadaver were findings: The main parotid duct originated two conducts: Left superior parotid duct and Left inferior parotid duct, is observed the criss-cross of the ducts, and then perforated the buccinator muscle and entered the oral cavity at a double parotid papilla containing a double opening, separated from each other in 0,98 mm. In the remaining  33 parotid regions (97.06%) the parotid duct is conformed to the classical descriptions given in anatomical textbooks. Conclusions: The parotid duct anatomy is important for duct endoscopy, lithotripsy, sialography and trans-ductal facial nerve stimulation in the early stage of facial palsy in some cases. The anatomical variations also has clinical importance for parotid gland surgery and facial cosmetic surgery. To keep in mind the parotid duct variation will reduce iatrogenic injury risks and improve diagnosis of parotid duct injury.


1997 ◽  
Vol 12 (5) ◽  
pp. 961-964 ◽  
Author(s):  
D. Rosenbaum ◽  
S. Holmes-Farley ◽  
W. Mandeville ◽  
M. Pitruzzello ◽  
D. Goldberg

Author(s):  
Andrew J. King ◽  
Jill Kohler ◽  
Cyra Fung ◽  
Zhengfeng Jiang ◽  
Allison Quach ◽  
...  

The majority of patients with chronic kidney disease (CKD) receiving dialysis do not reach target serum phosphorus concentrations, despite treatment with phosphate binders. Tenapanor is a non-binder, sodium/hydrogen exchanger isoform 3 (NHE3) inhibitor that reduces paracellular intestinal phosphate absorption. This pre-clinical study evaluated the effect of tenapanor and varying doses of sevelamer carbonate on urinary phosphorus excretion, a direct reflection of intestinal phosphate absorption. We measured 24-hour urinary phosphorus excretion in male rats assigned to groups dosed orally with vehicle or tenapanor (0.3 mg/kg/day) and provided a diet containing varying amounts of sevelamer (0-3% w/w). We also evaluated the effect of the addition of tenapanor or vehicle on 24-hour urinary phosphorus excretion to rats on a stable dose of sevelamer (1.5% w/w). When administered together, tenapanor and sevelamer decreased urinary phosphorus excretion significantly more than either tenapanor or sevelamer alone across all sevelamer dose levels. The Bliss statistical model of independence indicated that the combination was synergistic. A stable sevelamer dose (1.5% w/w) reduced mean (±standard error of the mean) urinary phosphorus excretion by 42±3% compared with vehicle; together, tenapanor and sevelamer reduced residual urinary phosphorus excretion by an additional 37±6% (P < 0.05). While both tenapanor and sevelamer reduce intestinal phosphate absorption individually, administration of tenapanor and sevelamer together results in more pronounced reductions in intestinal phosphate absorption than if either agent is administered alone. Further evaluation of combination tenapanor plus phosphate binder treatment in patients receiving dialysis with hyperphosphatemia is warranted.


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