Net Calcium Absorption Research Articles

The influence of citrate on the duodenal absorption of calcium in the rat

Using in situ perfusion in the rat, we studied the duodenal bidirectional fluxes (LP, lumen-to-plasma; PL, plasma-to-lumen) and the net absorption of calcium (Ca) at progressive molar citrate:Ca ratios (1:1, 2.1:1, 8.5:1) and three pH levels (pH 5.0, 6.25, 7.0) of the Ca-containing (4 mmol/liter) perfusion solution. Rats perfused with pH-adjusted, citrate-free solutions served as controls. LP-flux and net calcium absorption (net CaA) fell dose-dependently with increasing citrate concentrations. Also, at a given citrate:Ca ratio, LP-flux and net CaA fell with increasing pH of the perfusion solution. PL-fluxes did not change from control values, irrespective of the composition of the perfusion solution. The concomitant serum Ca and parathyroid hormone levels as well as blood pH and bicarbonate, were largely unchanged under any of the citrate-containing perfusion solutions. In conclusion, citrate inhibits duodenal CaA of the rat pH- and dose-dependently, without changing intestinal Ca secretion. This effect is not related to changes in the acid-base status or to suppressed parathyroid gland function of the animals and may be best explained by dose- and pH-dependent intraluminal complex formation between Ca and citrate.

Influence of the Disaccharide Lactitol on Intestinal Absorption and Body Retention of Calcium in Rats

Various sugars are known to stimulate intestinal calcium absorption by a mechanism that is still poorly understood. One of those, the disaccharide 4-gal-actosyl-sorbitol (lactitol), is only metabolized in the large intestine, where it is converted into acidic residues. We investigated the effect of this compound on net intestinal absorption and body retention of calcium in rats. Because dietary calcium is in a poorly absorbable form when it reaches the large intestine, attempts were made to modify the absorption of calcium present in the large intestine contents by administering lactitol. Net intestinal absorption and body retention of calcium were significantly increased by 2.5 g lactitol/(kg b.w.d) given by a gavage over a 7-d period. This was associated with a lower pH and a better availability to absorptive systems of calcium present in the large intestine contents. The results indicate that in rats lactitol given chronically increases net intestinal absorption of calcium with a subsequently more positive calcium balance.

Basal and hormone-activated calcium absorption in mouse renal thick ascending limbs.

These studies examined transepithelial routes of basal and hormone-activated calcium absorption in thick ascending limbs of Henle's loop perfused in vitro. Single cortical (cTAL) or medullary (mTAL) thick ascending limbs were dissected from kidneys of normal mice. Tubules were perfused at 37 degrees C at pH 7.4 in bicarbonate-buffered media for cTALs and in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solutions for mTALs. Calcium was determined by electrothermal atomic absorption spectrophotometry. External driving forces for calcium were eliminated by perfusing and bathing tubules with symmetric solutions containing identical calcium concentrations and by abolishing the transepithelial voltage (VT), by adding furosemide or bumetanide to the luminal perfusate. Basal calcium absorption averaged 60 X 10(-12) mol.s-1.cm-2 in cTAL. After addition of 1 U/ml parathyroid hormone (PTH)-(1-34), net calcium absorption increased to 162 X 10(-12) mol.s-1.cm-2 (P less than 0.05) with no change in VT. Similarly, addition of 10(-3) M dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) to external bathing solutions increased net calcium absorption to 201 from 70 X 10(-12) mol.s-1.cm-2 in control conditions (P less than 0.025). These results demonstrate that PTH, acting at least in part through cAMP, activates a cellular pathway for calcium absorption in cTAL. In segments of mTAL, calcium absorption was strictly voltage dependent: when VT was abolished, net calcium absorption fell to values indistinguishable from zero and was not altered in the presence of dibutyryl cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium transport in turtle bladder.

Unidirectional 45Ca fluxes were measured in the turtle bladder under open-circuit and short-circuit conditions. In the open-circuited state net calcium flux (JnetCa) was secretory (serosa to mucosa) and was 388.3 +/- 84.5 pmol.mg-1.h-1 (n = 20, P less than 0.001). Ouabain (5 X 10(-4) M) reversed JnetCa to an absorptive flux (serosal minus mucosal flux = -195.8 +/- 41.3 pmol.mg-1.h-1; n = 20, P less than 0.001). Amiloride (1 X 10(-5) M) reduced both fluxes such that JnetCa was not significantly different from zero. Removal of mucosal sodium caused net calcium absorption; removal of serosal sodium caused calcium secretion. When bladders were short circuited, JnetCa decreased to approximately one-third of control value but remained secretory (138.4 +/- 54.3 pmol.mg-1.h-1; n = 9, P less than 0.025). When ouabain was added under short-circuit conditions, JnetCa was similar in magnitude and direction to ouabain under open-circuited conditions (i.e., absorptive). Tissue 45Ca content was approximately equal to 30-fold lower when the isotope was placed in the mucosal bath, suggesting that the apical membrane is the resistance barrier to calcium transport. The results obtained in this study are best explained by postulating a Ca2+-ATPase on the serosa of the turtle bladder epithelium and a sodium-calcium antiporter on the mucosa. In this model, the energy for calcium movement would be supplied, in large part, by the Na+-K+-ATPase. By increasing cell sodium, ouabain would decrease the activity of the mucosal sodium-calcium exchanger (or reverse it), uncovering active calcium transport across the serosa.

Calcium transport across the colon ascendens and the influence of 1,25-dihydroxyvitamin D3 and dexamethasone.

Concentration dependence of unidirectional calcium fluxes across the rat colon ascendens were measured in a modified Ussing chamber. Both the mucosa (m) to serosa (s) and the s to m calcium flux exhibited saturation kinetics. The maximum transport rates and the affinity to the transporter of calcium was higher in the m to s direction than that from s to m, resulting in a remarkable net calcium absorption. The results obtained from measurements of unidirectional calcium fluxes in dependence on clamped transepithelial potentials showed that: (i) calcium transport in both direction had a voltage-independent component; (ii) the voltage-independent, i.e. non diffusive fraction of the m to s calcium flux was 3.2 times greater than that in the opposite direction; (iii) the voltage dependent, i.e. diffusional fraction of the m to s calcium flux, was about two times greater than the voltage-dependent fraction of the calcium flux in the s to m direction; and (iv) in the m to s direction 62%, and the s to m direction 73%, of the total unidirectional flux was voltage-dependent. Dexamethasone, known to enhance sodium and water absorption in the colon, had no significant influence on net calcium absorption but increased the unidirectional calcium fluxes in both directions. The increase in unidirectional calcium fluxes parallel to that of the extracellular marker mannitol suggests that dexamethasone has no influence on the transcellular calcium transport but increases the calcium flux along the paracellular way. Amiloride had no influence on the dexamethasone-induced changes of the epithelial electrical parameters as distinguished from the colon descendens.(ABSTRACT TRUNCATED AT 250 WORDS)

Thiazides stimulate calcium absorption in urinary bladder of winter flounder

Thiazides inhibit voltage-independent NaCl absorption in the urinary bladder of the winter flounder presumably by blocking an electroneutral mucosal Na/Cl co-transporter. As thiazides stimulate calcium absorption in mammalian distal convoluted tubule while inhibiting NaCl absorption, we studied the effects of hydrochlorothiazide (HCTZ) on unidirectional 45Ca fluxes and intracellular electrical potential in short-circuited bladders to examine possible mechanisms of HCTZ effects on calcium transport. Basal secretory calcium flux was, on average, slightly larger than absorptive flux, reflecting small net calcium secretion. Mucosal addition of HCTZ (10 −4 M) stimulated absorptive calcium flux by 46% while the secretory flux was unaltered. Thus, HCTZ tended to induce net calcium absorption. Pre-treatment with serosal ouabain (10 −4 M) attenuated the HCTZ-induced increase in absorptive calcium flux. Moreover, HCTZ hyperpolarized the mucosal membrane potential by 18% as measured by conventional open-tip microelectrodes. These effects of HCTZ are consistent with the hypothesis that HCTZ indirectly stimulates Na/Ca exchange located at the serosal membrane. In conclusion, HCTZ in flounder urinary bladder, as in mammalian distal convoluted tubule, simultaneously inhibits NaCl absorption and stimulates calcium absorption. This study expands on the functional similarities between the flounder urinary bladder and the mammalian distal convoluted tubule.

Calcium and magnesium transport and influence of 1,25-dihydroxyvitamin D3. In vivo perfusion study at the colon of the rat.

Calcium and magnesium transport at different luminal concentrations (1.25, 2.5, 5 and 10 mmol/l) and under the influence of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] were studied in vivo at the perfused colon of the rat. Net absorption of calcium and of magnesium were saturated with increasing concentrations of the perfusate. Net absorption of one ion was not affected by an increasing concentration of the other ion. 1,25(OH)2D3 (100 ng/day given subcutaneously for 4 days) stimulated net absorption of calcium and of magnesium. Presence or absence of calcium or magnesium, respectively, had no effect on the absorption of the other ion under 1,25(OH)2D3 stimulation. The results demonstrate that the colon of the rat is capable of absorbing calcium as well as magnesium. These observations suggest that calcium and magnesium in the rat colon are absorbed by two separate active transport mechanisms, which both are sensitive to 1,25(OH)2D3.

The influence of progressive hyperinsulinemia on duodenal calcium absorption in the rat

Using an in situ loop technique, we studied the influence of moderate hyperinsulinemia on the bidirectional fluxes [lumen-to-plasma (LP), plasma-to-lumen (PL)] and on the net absorption of calcium (Ca) in the duodenum of the rat. Under hyperinsulinemic euglycemic clamp conditions, three different steady-state plasma insulin levels (66 ± 16, 187 ± 13, 263 ± 24 μU/mL) were maintained by intravenous (IV) infusion of either 20, 40, or 60 mU/h of insulin. LP flux and net Ca absorption (CaA) increased significantly under all, while the PL flux was not changed by any of the three insulin doses. Under 40 and 60 mU/h of IV insulin, the individual plasma insulin levels and LP fluxes were positively and significantly correlated, suggesting a dose-dependent action of insulin on duodenal CaA. No significant changes were seen in plasma somatostatinlike immunoreactivity (SLI), parathyroid hormone (PTH), and serum Ca, while serum inorganic phosphate (Pi) and 1,25(OH) 2 vitamin D levels fell with increasing doses of IV insulin. It is concluded for the rat that (1) physiologic degrees of hyperinsulinemia enhance duodenal CaA by an as yet unknown mechanism, (2) this action seems to be independent of PTH and, (3) the role of 1,25(OH) 2 vitamin D in this context is poorly understood.

Effects of dietary sodium chloride loading on parathyroid function, 1,25-dihydroxyvitamin D, calcium balance, and bone metabolism in female rats during chronic prednisolone administration.

The effects of dietary sodium chloride supplements (8 g/100 g diet) on parathyroid function, serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], calcium balance, bone metabolism, and bone composition were studied in rats treated with prednisolone (2 mg/kg w X day) for 12 weeks. Animals on a low calcium diet (0.1% Ca) received the following treatments: group 1, control; group 2, NaCl; group 3, prednisolone; group 4, NaCl plus prednisolone. Parathyroid function was assessed indirectly from urinary cAMP excretion: bone resorption was estimated by studying urinary hydroxyproline excretion and mobilization of 45Ca from bone. Dietary salt loading increased the urinary excretion of calcium, 45Ca, cAMP, and hydroxyproline and raised serum 1,25-(OH)2D and net calcium absorption, but lowered calcium retention, femoral calcium, and total body calcium. Prednisolone slowed body growth and lowered net calcium absorption, calcium retention, femoral calcium, and total body calcium. Urinary calcium excretion was higher in rats receiving salt and prednisolone in combination than in animals taking salt without prednisolone, but other responses to salt and prednisolone were independent. Thus, salt and prednisolone each elicit osteopenia, and salt causes bone loss in rats receiving prednisolone. The osteopenic effect of salt is attributed to primary augmentation of urinary calcium excretion and secondary increases in PTH-medicated bone resorption. Although salt-treated rats have higher blood levels of 1,25-(OH)2D, bone loss occurs because alimentary calcium absorption is not elevated sufficiently to offset urinary calcium losses. Prednisolone lowers bone formation and net calcium absorption without lowering serum 1,25-(OH)2D values. The parathyroid-vitamin D axis remains intact in prednisolone-treated rats, as they show increases in PTH and 1,25-(OH)2D after salt treatment.

99 ASSESSMENT OF CA AND P REQUIREMENTS AND PREVENTION OF OSTEOPENIA IN VLBW INFANTS

Severe postnatal bone demineralization has now been recognized to be a common event in the VLBW infant because of calcium (Ca) and phosphorus (P) deficiency. Formula supplemented with Ca and P may not prevent this condition which is due to the wide variation in net calcium absorption. Hypothesis: Intrauterine bone mineral accretion rate will be achieved in VLBW infants postnatally when Ca and P are administered in sufficient quantity to result in a urinary excretion of both elements. Methods: To test this hypothesis we studied 18 periods of 3 weeks in 12 VLBW infants who were fed BM or formula supplemented with Ca-gluconate and Ca-glycerophosphate to produce a urinary excretion of 2-5 mmol/L Ca and P. The increase in bone mineral content (BMC, mg/cm) of the mid humerus measured by photonabsorptiondensitometry was assessed with respect to weight gain. Results: The median increase of BMC was 5.5 mg/cm per 100 g weight gain (range 2.7-9.9). This value is similar to the intrauterine accretion rate (4.6) which we have calculated from the BMC of newborn infants with birthweights between 800 and 4000 g (1). The mineral accretion rate, however was higher than the intrauterine rate in half of the study periods. Conclusion: Measurement of Ca and P in urine is a simple method by which individual requirements of Ca and P supplementation in VLBW may be accessed. Catch up mineralisation was observed in 9 of the babies. (1) Bone mineral content in appropriate and small for gestational infants: a reference for the evaluation of postnatal bone mineralization. Pediat Res 19:1116 (abstr.) (1985).

Response of spontaneously hypertensive rats to 1,25(OH)2D3 in vivo

Calcium absorption in spontaneously hypertensive rats (SHR) has been reported to be increased, decreased or not different from their normotensive Wistar Kyoto (WKy) control. One postulated reason for these conflicting results is an abnormal sensitivity to the intestinal effects of 1,25(OH)2D3 (1,25D3). Previous studies in everted duodenal sacs and perfused duodenum examined the acute response to 1,25D3 only in 12-week-old SHR, which however already had higher basal rates of calcium absorption. Inability to stimulate Ca absorption further was an unexcluded possibility. To test this hypothesis more vigorously, balance and in situ duodenal 45Ca uptake studies were performed in SHR and WKy using four separate protocols yielding the following results. First, in response to pharmacological doses of 1,25D3 (25 ng/100 g body wt/day X 3), four-week-old normotensive female SHR had higher net calcium absorption (41.4 vs. 31.1 mg/day; 61.6 vs. 48.1%), similar to the increases seen in the untreated state. These results suggest intrinsic epithelial differences independent of 1,25D3. Ca absorption was similarly higher in 1,25D3 treated male SHR (42.9 vs. 36.7 mg/day; 60.1 vs. 53.7%). Second, at 12 to 14 weeks of age, low doses of 1,25D3 (8 ng/100 g body wt/day X 6) stimulated net Ca absorption in the female SHR (33.0 to 39.1 mg/day), but not in WKy (26.8 to 29.3 mg/day). In the male, positive effects were again seen only in the SHR (25 to 45 mg/day). Third, in response to three weeks of dietary Ca deprivation, in situ duodenal 45Ca uptake, measured in the conscious awake state, was higher in 35-week-old SHR (70.9 vs. 53.0%).(ABSTRACT TRUNCATED AT 250 WORDS)

Direct effects of calcium channel blockers on duodenal calcium transport in vivo

The direct effects of verapamil, diltiazem and nifedipine on duodenal calcium transport were assessed in rats by the in vivo ligated loop technique, using luminal calcium concentrations at which active and passive transport mechanisms predominate (2 and 50 mM Ca, respectively). At 2 mM Ca, addition of verapamil (0.3–10 mM) to the luminal solution caused a concentration-dependent decrease in calcium lumen-to-plasma uptake and an increase in calcium plasma-to-lumen translocation, such that at 10 mM verapamil there was a net secretion of calcium into the duodenal lumen. In contrast, nifedipine (0.3–3 mM) was without effect on calcium transport, and diltiazem reduced calcium lumen-to-plasma uptake and net calcium absorption only at 10 mM, without influencing plasma-to-lumen translocation. The verapamil-induced increase in calcium plasma-to-lumen translocation was abolished by bile duct ligation. Calcium transport was unaffected by any calcium channel blocker at 50 mM luminal calcium. Thus, verapamil can directly influence active calcium translocation in the intestine, in vivo, and may affect calcium homeostasis during chronic oral treatment with this drug.

Glucose polymer increases jejunal calcium, magnesium, and zinc absorption in humans

The present study investigated the effect of glucose polymer on jejunal calcium, magnesium, and zinc absorption in eight normal subjects, using the triple-lumen intestinal perfusion technique. For each subject, a 30-cm segment of jejunum was perfused for 60 min each with two different test solutions. When 4 mM glucose polymer was perfused net calcium absorption increased by fourfold (95 vs 488 µmol/30 cm/h), and net jejunal uptake of magnesium (393 µmol/30 cm/h) was observed, as compared to net magnesium secretion in the absence of glucose polymer. In addition, coadministration of glucose polymer doubled net zinc absorption (13 vs 29 µmol/30 cm/h). The rate of water absorption increased from 49 to 111 ml/30 cm/h. No further change in jejunal water and mineral absorption was observed when glucose polymer in the perfusate was increased from 4 to 8 mM. These results suggest that glucose polymer may have potential as an agent to significantly enhance mineral absorption.

Effects of NaCl on Calcium Balance, Parathyroid Function and Hydroxyproline Excretion in Prednisolone-Treated Rats Consuming Low Calcium Diet

The short-term effects of dietary sodium chloride supplementation on calcium balance were examined in an animal model of corticosteroid-mediated osteoporosis. Changes in calcium and phosphate balance, parathyroid function and bone resorption elicited by salt supplements alone (8 g/100 g diet), prednisolone alone (2.2 mg/kg body wt per day) and both salt and prednisolone in combination were measured in rats consuming a low calcium diet (0.1% calcium) for 10 d. Parathyroid function was monitored by measuring urinary cyclic AMP excretion. Bone resorption was monitored by measuring urinary hydroxyproline excretion. Salt alone raised urinary calcium, cyclic AMP and hydroxyproline; prednisolone alone depressed net calcium absorption and urinary hydroxyproline but had no effect on urinary calcium. Salt and prednisolone each depressed calcium retention independently and together produced an additive adverse effect on calcium balance. Thus high dietary salt intakes augment urinary calcium loss, raise parathyroid activity, increase bone resorption and adversely affect calcium balance in prednisolone-treated growing rats with a restricted dietary calcium intake. These findings support the view that high salt intakes may exaggerate bone loss during chronic glucocorticoid therapy. Because people also develop osteoporosis during glucocorticoid therapy and respond to dietary salt supplements by increasing urinary calcium excretion and parathyroid hormone, high salt intakes may accelerate bone loss in patients receiving chronic glucocorticoid therapy. The beneficial effects of dietary salt restriction on the conservation of bone mass warrant investigation in these patients.

Acute effect of ethanol on intestinal calcium transport.

In vivo studies in rats demonstrated that acute intragastric administration of ethanol (3 g/kg BW) resulted in a reduced net absorption of fluid and calcium. Thirty minutes after an i.v. injection of 2 microCi 45Ca, the gastrointestinal 45Ca content in ethanol-treated rats was significantly higher than in controls indicating an increase in calcium secretion. The effect of ethanol on calcium movement was quantitated by measuring calcium fluxes across the in situ duodenal and ileal loops. Ethanol administration suppressed net duodenal calcium absorption by inhibiting the lumen to plasma flux of calcium. In contrast, ethanol enhanced plasma to lumen calcium flux in the ileum, resulting in net calcium secretion.

Effects of 1,25(OH)2D3 and calcium channel blockers on cecal calcium transport in the rat

To determine whether calcium transport across rat cecum is vitamin D dependent, we measured in vitro bidirectional calcium fluxes under short-circuited conditions across cecum from rats that were vitamin D deficient, vitamin D replete, or vitamin D deficient or vitamin D replete and injected with either 10, 25, or 75 ng of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] daily for 4 days before study. Vitamin D deficiency decreased net calcium absorption (Jnet) by reducing the mucosal-to-serosal absorptive flux (Jm----s) from 168 +/- 18 to 33 +/- 5 nmol X cm-2 X h-1 (mean +/- SE, P less than 0.0001). Twenty-five nanograms of 1,25(OH)2D3 raised Jm----s to 124 +/- 17 nmol X cm-2 X h-1, not different from values in vitamin D-replete rats. Although active calcium absorption by cecum appears to respond to vitamin D, calcium Jm----s is near maximal under normal conditions, and further stimulation follows only pharmacological doses of 1,25(OH)2D3. The in vitro addition of the calcium channel blocker verapamil (5 X 10(-5) M) to the mucosal side of cecum from vitamin D-replete rats reduced calcium Jm----s, but lower concentrations of verapamil or nitrendipine (10(-5) to 10(-9) M) did not reduce calcium Jm----s. The lack of inhibition by low concentrations of channel blockers suggest that the plasma membrane channels for calcium translocation across intestinal epithelium may not be analogous to voltage-dependent calcium channels in excitable tissue. The inhibition of cecal calcium transport that was blocked by high concentrations of verapamil may represent a nonspecific effect of the agent.

Intestinal Calcium Absorption Is Enhanced D-Glucose in Diabetic and Control Rats

The effect of glucose on intestinal absorption of calcium was studied in the jejunum and ileum of control, diabetic (streptozotocin-induced), and insulin-treated diabetic rats. Intestinal absorption was determined in vivo using an in situ one-pass perfusion technique. In the jejunum of control and diabetic rats, net absorption and unidirectional lumen to mucosa flux of calcium and net absorption of water were significantly greater during perfusion of an isotonic NaCl solution, containing 15 mmol/L of glucose, than during perfusion of the same solution containing 15 mmol/L of mannitol instead of glucose. To determine if net absorption of calcium and water were related, the jejunum was perfused with a hypotonic solution (260 mosmol/kg) in separate groups of rats. Although net absorption of water was equivalent during perfusion of the hypotonic solution to that noted during perfusion of the isotonic glucose-containing solution, rate of absorption of calcium was not enhanced. Thus, it appeared that, if the enhancement in absorption of calcium by glucose was an effect on the passive absorption of calcium, it was through a mechanism not related to passive absorption of water. As expected, jejunal absorption of calcium was lower in diabetic than in control rats. Because in diabetic rats the metabolism of vitamin D to its active metabolite, 1,25-dihydroxy vitamin D, is defective, the enhancement in absorption of calcium by glucose did not appear to be due to a mechanism influenced by vitamin D metabolism. In the ileum, rate of absorption of calcium was lower than in the corresponding jejunum and was not significantly altered by the presence of glucose in the perfusion solution, by perfusion of a hypotonic solution, or by the diabetic state. The mechanism of action of glucose on calcium absorption in the jejunum needs to be studied further.

The effects of sodium fluoride, calcium phosphate, and vitamin D 2 for one to two years on calcium and phosphorus metabolism in postmenopausal women with spinal crush fracture osteoporosis

Calcium and phosphorus balances and 47Ca turnover studies were performed before and after 12–27 months of daily treatment with sodium fluoride (60 mg), calcium (30–45 mmol), phosphate (29–44 mmol), and vitamin D 2 (18,000 IU) in 20 postmenopausal women with spinal crush fracture osteoporosis. Before treatment the mean calcium balance (−1.6 mmol Ca/day) was negative ( P < 0.05), whereas the mean phosphorus balance ( −1.6 mmol P day ) did not differ from zero( P > 0.10). The treatment induced an increase in calcium absorption ( P < 0.01) with an unchanged renal excretion and dermal loss of calcium and an increase ( P < 0.02) in calcium balance, which became positive ( P < 0.01) ( + 3.3 mmol Ca day ). This enhancement in calcium balance was obtained by the combined effects of an increase ( P < 0.05) in bone mineralization rate and a decrease ( P < 0.05) in bone resorption rate. The observed increase in net phosphorus absorption ( P < 0.001) was more pronounced than the increase in renal excretion of phosphorus ( P < 0.001), and the phosphorus balance therefore increased ( P < 0.001) and became positive ( P < 0.001). A positive correlation was observed between net calcium and net phosphorus absorption ( r = 0.065; P < 0.001) in the 32 studies where both calcium and phosphorus balance data were available. Furthermore, a positive correlation ( r = 0.61; P < 0.05) was found between the changes in net calcium and net phosphorus absorption during treatment. The results indicate that the combined treatment with sodium fluoride, calcium, phosphate, and vitamin D 2 induces a positive calcium and phosphorus balance in postmenopausal women with osteoporosis.

Interrelation of cortisone and 1,25 dihydroxycholecalciferol on intestinal calcium and phosphate absorption.

The interrelation of glucocorticoids and 1,25 dihydroxycholecalciferol (1,25(OH)2D3) on intestinal calcium and phosphate absorption was investigated. The active and passive transport of calcium and phosphate was evaluated by the in situ intestinal loop technique. Administration of cortisone resulted in a decrease of the luminal fluid and an increase of the luminal calcium and phosphate concentration. Under active transport conditions, administration of cortisone resulted in a decrease of net calcium absorption through two mechanisms: (1) depressed vitamin D-dependent calcium absorption, (2) increased vitamin D-independent calcium backflux. The enhancement of bidirectional phosphate flux by cortisone was independent of 1,25(OH)2D3. An enhancement of water movement by cortisone resulted in an increase of luminal calcium and phosphate concentration which favors the passive diffusion of these ions. Enhanced calcium diffusion by cortisone compensates for the inhibitory effect of cortisone on vitamin D-dependent calcium transport. However, enhanced phosphate diffusion by cortisone is additive to the effect of 1,25(OH)2D3.

Calcium transport in the rabbit superficial proximal convoluted tubule.

Calcium transport was studied in isolated S2 segments of rabbit superficial proximal convoluted tubules. 45Ca was added to the perfusate for measurement of lumen-to-bath flux (JlbCa), to the bath for bath-to-lumen flux (JblCa), and to both perfusate and bath for net flux (JnetCa). In these studies, the perfusate consisted of an equilibrium solution that was designed to minimize water flux or electrochemical potential differences (PD). Under these conditions, JlbCa (9.1 +/- 1.0 peq/mm X min) was not different from JblCa (7.3 +/- 1.3 peq/mm X min), and JnetCa was not different from zero, which suggests that calcium transport in the superficial proximal convoluted tubule is due primarily to passive transport. The efflux coefficient was 9.5 +/- 1.2 X 10(-5) cm/s, which was not significantly different from the influx coefficient, 7.0 +/- 1.3 X 10(-5) cm/s. When the PD was made positive or negative with use of different perfusates, net calcium absorption or secretion was demonstrated, respectively, which supports a major role for passive transport. These results indicate that in the superficial proximal convoluted tubule of the rabbit, passive driving forces are the major determinants of calcium transport.