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Net Ca2+ and Mg2+ absorption rates were measured in vivo from buffer solutions placed in the washed reticulo-rumen, isolated in situ in 30 conscious, trained sheep. An increase in concentration of short chain fatty acids (SCFA) in the buffer, over the range 0–50 mM, was shown to stimulate the net rates of absorption of Ca2+ and Mg2+ ions from the rumen. Similarly, the results of in vitro experiments, carried out with ovine rumen epithelium mounted in short-circuited Ussing chambers, showed that the absence of SCFA from the chamber fluid resulted in a reduction in Jnet Ca2+ caused by reduced flux of Ca2+ ions in the mucosal to serosal direction (Jms Ca2+). The addition of 1 mM acetazolamide, an inhibitor of carbonic anhydrase, to the ruminal buffer used in the in vivo experiments led to significant reductions in the net absorption rates of Ca2+and Mg2+ ions in the presence of SCFA (50 mmol l-1) but not in the absence of SCFA. However, in the in vitro experiments, the addition of 60 μM ethoxyzolamide had no significant effect on Jnet Ca2+. A reduction in pH of the intraruminal buffer in vivo from 6.8 to 5.4 led to significant increases in the net absorption rates of Ca2+and Mg2+ ions, an effect which was duplicated for Ca2+ in preliminary in vitro experiments in which the pH of the mucosal buffer was reduced from 7.4 to 5.4. This stimulatory effect was confined to Jms Ca2+ and Jnet Ca2+. Ussing chambers were also used to demonstrate that Jnet Ca2+ was reduced by a high transmural potential difference (PD), caused by voltage clamping, independently of the mucosal K+ concentration. Both unidirectional Ca2+ fluxes consisted of a PD-dependent and a K+-insensitive PD-independent component. The latter may be represented by a Ca2+/2H+ antiporter. It is postulated that SCFA, and to a lesser extent H2CO3, can stimulate Jms Ca2+ by activation of an apical Ca2+/2H+ antiporter through the provision of protons within the ruminal epithelial cell. A mild reduction in ruminal pH may also lead to a similar stimulation of this putative electroneutral exchange. [ABSTRACT FROM AUTHOR]

The net absorption rates of strontium ions from the ovine reticulo-rumen, isolated in situ in trained conscious animals, were measured under controlled conditions. A linear positive response was obtained from the addition of Sr2+ ions to the artificial rumen fluid. This increase in the absorption of Sr was reflected in an increase in the plasma Sr concentration. In contrast to the discrimination observed elsewhere in favour of the absorption of Ca relative to Sr, the absorption rate of Sr from the reticulo-rumen was significantly greater than that of Ca, from solutions containing the same molar concentration. A graded increase in the Sr concentration in the ruminal fluid from 1 mmol/l to 4 mmol/l led to a corresponding reduction in the absorption rate of Ca but an increase in that of phosphate. The latter result is similar to that observed when the intra-ruminal concentration of Ca2+ ions is increased. It is suggested that Ca and Sr share a common pathway for absorption from the reticulo-rumen and that this may involve coupling with the absorption of phosphate ions. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine whether total serum calcium, parathyroid gland structure, and/or levels of parathyroid hormone, 1,25 and 24,25 DHCC, are altered in pigs with dental and skeletal fluorosis. Eight experimental animals receiving 2 mg F-/kg b.w. per day from age 8-14 months were compared with eight controls. Concentrations of plasma fluoride and total plasma calcium were assessed at intervals throughout the experiment and during a 48 hour period at day 110-111 of the experiment. At the same time, concentrations of immunoreactive parathyroid hormone were measured using a homologous labeled antibody for porcine hormone, and a radioimmunoassay was used to assess concentrations of 1,25 DHCC and 24,25 DHCC. Parathyroid tissue volumes were assessed at the end of the experiment by quantitative histology using volumetry and point counting. Plasma fluoride increased from 0.0007 +/- 0.0001 mmol/liter to 0.0127 +/- 0.002 mmol/liter in pigs receiving fluoride. In spite of this increase, total plasma calcium remained the same throughout the experiment. Volumes of parathyroid tissue, and levels of circulating parathyroid hormone 1,25 DHCC and 24,25 DHCC, were not significantly changed. It was therefore concluded that disturbance of calcium homeostasis is not an obligatory finding in dental and skeletal fluorosis and consequently does not play an essential role in the pathogenesis of these hard tissue lesions. [ABSTRACT FROM AUTHOR]

In late pregnancy the sheep fetus requires 3 g of calcium per day, all of which must be transported across the trophoblast epithelium of the placenta. Such high levels of calcium transport across other epithelia are normally associated with the presence of calbindin-Dor . Our immunocytochemical results show that ovine, bovine and caprine interplacentomal trophoblast have high levels of calbindin-D, about eight to ten times more than in the placentomal region. The protein is detectable only in the uninucleate trophoblast cells in sheep and goat, the frequent binucleate cells show none. The calbindin-Dis also present in the maternal glandular epithelium but not the surface epithelium of the uterus. The cellular distribution of the calbindin-Dimmunoreactivity suggests a soluble protein homogenously distributed through cytosol and nucleoplasm but absent from all organelles and intercellular spaces. In contrast, the uterine milk protein(s) are localised in Golgi cisternae and secretory vesicles in gland cells and in apical small endocytic vesicles and lysosomes in the uninucleate trophectodermal cells. The distribution of calbindin-Dsupports the concept that it mediates the high calcium flux by facilitated diffusion and not via any vesicular, membrane-bounded system. [ABSTRACT FROM AUTHOR]

SUMMARY 1. The oral administration of polysodium metaphosphate in the rat causes an increase in the incidence of the scattered foci of calcification found in the kidneys of a small proportion of normal animals. 2. No abnormal calcification occurred in other tissues. 3. Mortality was not increased. 4. Growth was not affected. 5. Fertility, pregnancy, and lactation appear to be unaffected. 6. The determination of the dosage which gives the maximum suppression of urinary calculus formation for the minimum increase in renal parenchymal calcification is discussed. We wish to thank Professor L. N. Pyrah and Professor M. F. A. Woodruff for providing facilities for these experiments in their laboratories at Leeds University and Edinburgh University respectively, the Secretary of State for Scotland for the grant of financial assistance, and Messrs Albright & Wilson Ltd. for the supplies of polysodium metaphosphate. [ABSTRACT FROM AUTHOR]

SUMMARY 1. The theoretical basis of the use of orally administered polysodium metaphosphate to suppress stone formation in the urinary tract is discussed. 2. It is shown that the addition of polysodium metaphosphate to urine in vitro can prevent calcium oxalate precipitation. 3. A method of estimating the amount of polysodium metaphosphate excreted in the urine is described. 4. The stone-suppressing action of oral polysodium metaphosphate in rats is confirmed. 5. This action appears to be independent of changes in the pH or dilution of the urine. [ABSTRACT FROM AUTHOR]

SUMMARY A case of polycystic kidneys is described for which an auxiliary kidney in the form of an isolated loop of ileum was prepared. Irrigation of this loop usually resulted in clinical improvement, and the investigations carried out suggest that this was brought about by the removal of some toxic metabolite, possibly nitrogenous in character. [ABSTRACT FROM AUTHOR]

Summary The mammalian fetus is maintained hypercalcaemic relative to its mother primarily by the action of a placental calcium pump located in the basal plasma membrane of the trophoblast. It is suggested that the activity of this pump is stimulated by a mid-molecular fragment of parathyroid hormone-related protein [PTHrP(38-94NH [ABSTRACT FROM AUTHOR]