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At least 19 recordsLinked to original sources
PubMed1975

The role of the parathyroids for the adaptation to a low calcium intake. 4. The long-term effect of parathyroidectomy on the adaptation to a low calcium intake in adult rats with special reference to calcium metabolism.

One-year-old selectively parathyroidectomized rats showed, on a normal dietary intake of calcium, phosphorus and vitamin D, a reduction in plasma calcium to below 4.1 mEq./1 in 86 per cent and on restricted calcium intake in 100 per cent. On the normal level of dietary calcium, normalization of plasma calcium occurred 17 per cent within 8 weeks and in another 40 per cent between the 8th and 27th week of observation while on the low level only 10 per cent of the animals normalized their plasma calcium and first after the long-term period of observation. This was most probably accomplished by successively restored parathyroid activity from aberrant parathyroid tissue as deducted from data regarding the metabolism of calcium, magnesium and inorganic phosphate. Adaptation, viz. normalization of plasma calcium, was brought about by mobilization of skeletal calcium with resulting osteoporosis, as reported in our previous study on the same animals. Intestinal net absorption of calcium showed no significant difference between normocalcemic normophosphatemic intact and hypocalcemic hyperphosphatemic parathyroidectomized animals at the respective level of dietary calcium. Thus, parathyroidectomized animals with persistently reduced plasma calcium showed a normal adaptory increase in intestinal calcium absorption upon chronically restricted calcium intake. In the discussion of the regulation of this adaptory system the possible effects of the plasma concentrations of both calcium and inorganic phosphate upon the intracellular Ca22+concentration in the kidney tubules must be considered. Plasma magnesium did not appear to have a primary influence. Intestinal absorption of inorganic phosphate was not dependent upon the presence of the parathyroids but followed that of calcium suggesting a regulation by the action of 1,25-dihydroxycholecalciferol.

Adaptation, Physiological↗
PubMed1975

The role of the parathyroids for the adaptation to a low calcium intake. 3. The long-term effect of parathyroidectomy on the adaptation to a low calcium intake in adult rats with special reference to plasma calcium, bone tissue and adrenal glands.

One-year-old selectively parathyroidectomized rats responded with a plasma calcium reduction to below 4.1 mEq./1 in 86 per cent at a normal and in 100 per cent at a low dietary calcium intake. Among the former, 17 per cent normalized their plasma calcium level within 8 weeks and another 40 per cent between the 8th ana 27th week of observation. Among the latter, only 10 per cent showed a normalization and first after the long-term period of observation. On the normal level of dietary calcium the parathyroidectomized animals with persistently reduced plasma calcium showed a significantly increased bone mass which was paradoxical in view of their inability of adaptation. On the low level of dietary calcium a normal bone resorptive activity was maintained despite parathyroidectomy possibly through the action of increased levels of 1,25-dihydroxycholecalciferol provoked by the profoundly reduced plasma calcium. This was, however, insufficient for adaptation and no osteoporosis developed. For the adaptation to a reduced calcium intake skeletal calcium reserves had to become mobilized through the action of the parathyroids with resulting osteoporosis. This was brought about by increased mobilization of skeletal calcium with resulting osteoporosis, a phenomenon which could be seen also among the parathyroidectomized animals on a low dietary calcium and with a normalized plasma calcium level. This osteoporosis was similar to that found in the calcium deficient intact animals. The described bone changes were progressing in character and there was no major influence by any eventual effect on bone growth. At histological and morphometric analyses of the adrenal cortex no apparent changes were found after parathyroidectomy.

Adaptation, Physiological↗
PubMed1976

[Studies on calcium absorption out of a calcium-vitamin-D-preparation using calcium-47 (author's transl)].

Calcium absorption in man was studied by means of labelling an ampoule of Frubiase Calcium forte with calcium-47. For comparative purpose a solution containing the same amount of calcium salts as the ampoule was labelled as well. Already 10 minutes after oral administration of Ca-47 in 10 ml of Frubiase Calcium forte radioactivity was statistically significant measurable in blood. At the same time there was no significant radioactivity demonstrable out of the calcium salt solution. Between 45 and 120 minutes following oral application of the isotope both groups showed a statistically significant difference concerning the measurable blood activity. The Frubiase Calcium forte values were always higher, especially one and two hours after administration of the radiocalcium (up to 40%). The levels at these times correlate well with the total calcium absorption. Measurements over the compact bone region of the ankle demonstrated significantly higher values of calcium-47 in case of Frubiase Calcium forte compared with the calcium salt solution. These findings indicate in the case of Frubiase Calcium forte a higher bone mineral accretion. There is a good direct proportionality between the amount of these values and the total calcium absorption.

Adult↗
PubMed1992

Prevention of calcium overload and down-regulation of calcium channels in rat heart by SR 33557, a novel calcium entry blocker.

The effect of SR 33557, a novel calcium entry blocker, on calcium overload, and regulation of calcium channels and beta-adrenergic receptors was investigated in the rat heart. Calcium overload and infarct-like lesions were produced by a large dose of isoproterenol (40 mg/kg, subcutaneously) to rats. Calcium overload was maximal 8 hours after administration of isoproterenol (control: 5.7 mmol Ca2+/kg dry weight, isoproterenol: 34.9 mmol Ca2+/kg dry weight). At that time, a decrease in the total number of beta-adrenergic receptors (-27%) and calcium channels (-20% and -23%) was observed. Intravenous injection of SR 33557 (0.5-10 mg/kg), 30 minutes before administration of isoproterenol, attenuated the increase in calcium content in a dose-related manner, such that 5 mg/kg SR 33557 reduced calcium overload by 50%. At this dose, SR 33557 had no effect on the number of beta-adrenergic receptors but prevented the decrease in the number of calcium channels. The total number of binding sites and the dissociation constants of each radioligand were estimated from saturation isotherms. The dissociation constants were unchanged when animals given isoproterenol or SR 33557 and isoproterenol were compared to the control group. The results indicate that SR 33557 is able to protect against the calcium overload induced by sympathetic over-stimulation. This over-stimulation of the sympathetic system causes a down-regulation of the number of active beta-adrenergic receptors and calcium channels. The down-regulation of calcium channels is selectively reduced by earlier administration of SR 33557.

Animals↗
PubMed1979

The interaction between dietary calcium and gonadal hormones in their effect on plasma calcium, bone, 25-hydroxycholecalciferol-1-hydroxylase, and duodenal calcium-binding protein, measured by a radioimmunoassay in chicks.

Male chicks, fed low, normal, or high calcium- and cholecalciferol-containing diets for 14 days, were given three combined injections of 17 beta-estradiol and testosterone (7 and 2.4 mg/kg/dose, respectively) or the vehicle alone, at 3-day intervals. The hormonal treatment resulted in increased plasma calcium and medullary bone calcium concentrations, independently of the dietary calcium intake. Kidney 25-hydroxycholecalciferol-1-hydroxylase and duodenal calcium-binding protein were increased in response to gonadal hormones. The magnitude of this response markedly diminished with increased calcium intake and almost completely disappeared in chicks fed the high calcium diet. The results suggest that the increases in plasma calcium and medullary bone formation due to gonadal hormones are independent of calcium intake while the effect of hormones on duodenal calcium-binding protein and the 25-hydroxycholecalciferol-1-hydroxylase activity appears to be mediated through the change in calcium needs due to medullary bone formation.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1975

Studies in calcium metabolism. II. Effects of low calcium and variable protein intake on human calcium metabolism.

Six healthy males consumed diets containing about 0.1 g calcium/day at three levels of protein intake: 0.9, 12, and 24 g nitrogen/day. Daily urinary calcium excretion on the 0.9 nitrogen diet was 51 mg, 99 mg on the 12 g nitrogen diet, and 161 mg on the 24 g nitrogen diet. A calcium supplement of 0.9 g for four subjects on the 12 g nitrogen diet caused an increase in urinary calcium from 68 to 160 mg/day. Varying the calcium and protein intake had no effect on dermal calcium loss or serum calcium. Five subjects had the least negative calcium balance on the 12 g nitrogen diet. Increase in urinary calcium is not likely to result solely from enhancement of intestinal calcium absorption. Our data suggest that increased glomerular filtration with possible inhibition of renal tubular reabsorption of calcium may be an additional mechanism responsible for the calciuretic effect during high-protein intake.

Adult↗
PubMed1975

Calcium distribution in islets of Langerhans: a study of calcium concentrations and of calcium accumulation in B cell organelles.

Calcium concentrations of various pancreatic B cell organelles have been determined by X-ray microanalysis of areas of frozen sections of unfixed rat islets of Langerhans. Highest concentrations were detected in storage granules and in mitochondria, although calcium was also present in nuclei, in areas of endoplasmic reticulum and of cytoplasm. Accumulation of 45Ca by isolated organelles has been studied in homogenates and isolated subcellular fractions of rat islets of Langerhans. In the presence of a permeant anion (oxalate or phosphate), accumulation of 45Ca into mitochondria and microsomes was strongly stimulated by ATP. This net uptake was diminished during incubation of homogenates or of a mitochondria plus storage granule-rich fraction in the presence of cyclic AMP, dibutyryl cyclic GMP; 2:4-dinitrophenol or of ruthenium red. Investigations of the characteristics of 45Ca accumulation by homogenates prepared from storage granule-depleted islets showed no differences from those of normal islets, suggesting that the granules do not represent an important labile pool of calcium. With the exception of cyclic AMP and cyclic GMP none of the insulin secretagogues tested (glucose, leucine, arginine, adrenalin, noradrenalin, theophylline, glibenclamide) altered calcium accumulation by islet homogenates. On the basis of absolute calcium levels and of 45Ca uptake studies it is concluded that islet B cells contain a readily exchangeable mitochondrial calcium pool, and an endoplasmic reticulum pool containing a lower concentration of calcium which is also readily exchangeable. The storage granules, despite their high calcium content, do not appear to constitute a labile pool. It seems likely that the labile mitochondria and endoplasmic reticulum pools play a predominant role in the regulation of cytoplasmic free calcium levels, which may in turn be important in the regulation of rates of insulin secretion.

Adenosine Monophosphate↗
PubMed1992

Enhanced spontaneous calcium efflux and decrease of calcium-dependent calcium release from the isolated perfused heart of spontaneously hypertensive rats.

OBJECTIVE: The aim of this study was to clarify the further details of calcium handling in hypertension. DESIGN: By preserving the physiological environment of cell membrane, whole hearts were used for comparison of calcium flux between spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. METHODS: Hearts from SHR and WKY rats were perfused with Krebs-Henseleit solution under constant flow and the effluent collected. RESULTS: After labelling of the heart with 45Ca2+ (100 mumol/l), 45Ca2+ binding was found to be saturated, and washing with calcium-free perfusion solution showed two exponential curves for calcium dissociation, indicating a fast (alpha-) and slow (beta-) phase. The half-lives of the beta-phase for both 4- and 8-week-old SHR were significantly shorter than those for age-matched WKY. Also in this phase, infusion of non-radioactive Ca2+ caused a transient dose-dependent release of 45Ca2+. A significant reduction in the amount of 45Ca2+ release induced by 2 mmol/l Ca2+ was observed in both 4- and 8-week-old SHR compared with age-matched WKY rats. Infusion of lanthanum, caffeine, ionomycin (calcium ionophore) and treatment of the hearts with ethyleneglycol-bis-(beta-aminoethylether)-N,N,N,',N'-tetraac etic acid did not alter 45Ca2+ release by non-radioactive Ca2+. From these observations, 45Ca2+ is presumably released from the intracellular calcium pool, and not from extracellular binding sites or sarcoplasmic reticulum. CONCLUSIONS: These findings suggest that an abnormal calcium-handling defect (enhanced calcium efflux and reduction of membrane-bound Ca2+) exists under physiological conditions before and after the onset of hypertension, and that this may be a primary characteristic of SHR.

Aging↗
PubMed1991

Glycochenodeoxycholic acid inhibits calcium phosphate precipitation in vitro by preventing the transformation of amorphous calcium phosphate to calcium hydroxyapatite.

Calcium hydroxyapatite can be a significant component of black pigment gallstones. Diverse molecules that bind calcium phosphate inhibit hydroxyapatite precipitation. Because glycine-conjugated bile acids, but not their taurine counterparts, bind calcium phosphate, we studied whether glycochenodeoxycholic acid inhibits calcium hydroxyapatite formation. Glycochenodeoxycholic acid (2 mM) totally inhibited transformation of amorphous calcium phosphate microprecipitates to macroscopic crystalline calcium hydroxyapatite. This inhibition was not mediated by decreased Ca2+ activity. Taurocholic acid (2-12 mM) did not affect hydroxyapatite formation, but antagonized glycochenodeoxycholic acid. Both amorphous and crystalline precipitates contained a surface fraction relatively rich in phosphate. The surface phosphate content was diminish by increasing glycochenodeoxycholic acid concentrations, and this relationship was interpreted as competition between bile acid and HPO4(-4) for binding sites on the calcium phosphate surface. A phosphate-rich crystal surface was associated with rapid transition from amorphous to crystalline states. These results indicate that glycochenodeoxycholic acid prevents transformation of amorphous calcium phosphate to crystalline hydroxyapatite by competitively inhibiting the accumulation of phosphate on the crystal embryo surface.

Calcium↗
PubMed1992

Control of predialytic hyperphosphatemia by oral calcium acetate and calcium carbonate. Comparable efficacy for half the dose of elemental calcium given as acetate without lower incidence of hypercalcemia.

Since Mai et al. found, with the intestinal lavage technique, that the same dose of elemental calcium given as acetate (Ca Ac) complexed in the gut of uremic patients twice as much phosphate as calcium carbonate (CaCO3) while inducing a rather low calcium absorption, we wanted to see if half the dose of elemental calcium given as Ca Ac could control, on medium term, the predialysis plasma phosphate as well as CaCO3 while inducing less frequent hypercalcemia. This was evaluated in a cross-over study of 3 periods of 10 weeks according to the sequence Ca Ac, CaCO3 and Ca Ac, in 12 compliant patients on chronic dialysis previously treated by CaCO3. Because of poor tolerance of Ca Ac during the first period, 4 patients were excluded and the results were assessed only on the 8 patients who completed the study. For half the doses of elemental calcium (620 +/- 250 mg versus 1,310 +/- 560 mg versus 710 +/- 200 mg/day), Ca Ac allowed the same control of predialytic hyperphosphatemia (1.67 +/- 0.34; 1.74 +/- 0.32; 1.75 +/- 0.38) with paradoxically comparable normal mean plasma calcium concentration (2.61 +/- 0.14; 2.56 +/- 0.13; 2.55 +/- 0.14 mmol/l). Plasma alkaline phosphatases and intact PTH concentrations remained also stable during the 3 periods. The frequency of hypercalcemia greater than 2.75 mmol/l (12; 9; 20%) and of hyperphosphatemia greater than 2 mmol/l (17; 22; 27%) were comparable with the 2 treatments. In conclusion, Ca Ac controls predialytic hyperphosphatemia as efficiently as CaCO3 for half the dose of elemental calcium without, however, decreasing the frequency of hypercalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1975

Calcium uptake and calcium release by subcellular fractions of smooth muscle. II. Kinetics of calcium uptake by microsomes and mitochondria from pig coronary artery and guinea pig ileum.

Calcium uptake by the microsomal and mitochondrial fractions of pig coronary artery and guinea pig ileum was studied in the presence of ATP, ATP plus oxalate and without ATP and oxalate. Microsomes and mitochondria of both smooth muscles were found to be unable to accumulate appreciable amounts of calcium in the absence of ATP. Oxalate noticeably stimulated the calcium uptake of the mitochondrial fraction from pig coronary artery but had little effect on calcium uptake by the microsomal fraction of this smooth muscle. The calcium uptake of microsomes and mitochondria from guinea pig ileum was not or only slightly enhanced by oxalate. There are typical kinetics regarding the time course and the extent of calcium uptake by microsomes and mitochondria from pig coronary artery and guinea pig ileum. In comparison, considerable qualitative and quantitative differences between both smooth muscles are observed. The high ATP-dependent calcium uptake capacity of the mitochondria from pig coronary artery and guinea pig ileum are a further argument for the hypothesis that these organelles may play an important role in the contraction-relaxation mechanism of smooth muscle.

Adenosine Triphosphate↗
PubMed1975

Radioimmunoassay studies of intestinal calcium-binding protein in the pig. I. Identification of intestinal calcium-binding protein in blood and response to a low calcium diet.

We have developed a radioimmunoassay for porcine intestinal calcium-binding protein (CaBP) and have used it to detect CaBP in pig plasma. Plasma CaBP is identical to intestinal CaBP on the basis of immunological activity, molecular size, and molecular charge properties. The plasma CaBP concentration was greater in the portal blood than in mixed venous blood, suggesting that blood CaBP originates in the gut. Two of four 15-week-old littermate pigs were placed on a low calcium diet (0.15% calcium, 0.65% phosphorus) and two on a control diet (0.65% calcium, 0.65% phosphorus). After 2 weeks, the entire small intestine was removed and divided into nine 1.8-m segments. CaBP was assayed in both plasma and intestinal mucosa. When the two pigs on a low calcium diet were compared with two control pigs, there was a general increase in immunoreactive CaBP in both plasma and intestinal mucosa. However, there was no increment in immunoreactive CaBP in the first 1.8-m segment of small intestine. Seventy-one percent of the increment in CaBP occurred distal to the first two segments. The largest fractional low calcium diet effect occurred in the ileum. The mean CaBP concentration for the total small intestine increased by a factor of 1.9. The plasma CaBP concentration increased by a factor of 2.6. In these pigs, plasma CaBP was a more reliable indicator of change in CaBP status than was the measurement in the proximal gut segment which contained the duodenum. The assay of CaBP in blood is convenient and may obviate the sampling errors inherent in intestinal biopsy.

Animals↗
PubMed1976

The subcellular localization of calcium in vertebrate smooth muscle; calcium-containing and calcium-accumulating structures in muscle cells of mouse intestine.

The intracellular localization of calcium by means of cytochemical techniques was studied in smooth muscle cells of mouse intestine. When the lead acetate method according to Carasso and Favard (1966) was used calcium was found in mitochondria and sarcoplasmic reticulum and occasionally between the myofilaments. The active ATP-dependent accumulation of calcium into cell structures was investigated by the oxalate method (Heumann and Zebe, 1967). After appropriate treatment the only structures of smooth muscle cells which contained calcium oxalate (identified by microprobe analysis) were elements of the sarcoplasmic reticulum. The results are discussed in relation to the role of calcium in the control of muscle activity during the contraction-relaxation cycle.

Acetates↗
PubMed1991

8-Diethylamino-octyl-3,4,5-trimethoxybenzoate, a calcium store blocker, increases calcium influx, inhibits alpha-1 adrenergic receptor calcium mobilization, and alters iodide transport in FRTL-5 rat thyroid cells.

8-Diethylamino-octyl-3,4,5-trimethoxybenzoate (TMB-8) is known to inhibit mobilization of calcium from intracellular stores but, more recently, other cellular effects have been described. In the present study, the effects of TMB-8 on cytosolic free calcium [Ca2+]i levels in FRTL-5 rat thyroid cells were determined using the fluorescent dye, Indo-1. TMB-8 increased [Ca2+]i in a dose-dependent manner, with a maximum rise from 120 +/- 7 nM to 229 +/- 16 nM (90 +/- 5% increase) at 5 x 10(-4) M. This effect was considerably reduced in Ca2+ free buffer, demonstrating a dependency upon extracellular calcium influx but not upon membrane potential and which did not involve the Na+/Ca2+ exchanger. In Ca2+ free buffer TMB-8, at a dose which did not affect [Ca2+]i, completely prevented norepinephrine (10(-5) M) from mobilizing intracellular Ca2+. To determine whether TMB-8 affected differentiated functions, iodide uptake and efflux studies were performed with 125I. TMB-8 (10(-4) M) inhibited iodide uptake by approximately 40% without affecting efflux. At 10(-3) M TMB-8, efflux was also enhanced. These studies demonstrate that TMB-8 has at least two effects on [Ca2+]i, promoting calcium influx and preventing alpha-1 adrenergic mobilization from intracellular stores. TMB-8 also has multiple effects on 125I transport, both inhibiting influx and increasing efflux. The results emphasize the importance of characterizing the behavior of this compound in any cell system before using it as a biological probe.

Animals↗
PubMed1992

Effect of vitamin D3 administration on the serum calcium and inorganic phosphate levels of the freshwater catfish, Heteropneustes fossilis, maintained in artificial fresh water, calcium-rich fresh water, and calcium-deficient fresh water.

Freshwater catfish, Heteropneustes fossilis, were injected daily intraperitoneally either with vehicle (0.05 ml of 95% ethanol/100 g body wt) or vitamin D3 (50 I.U./100 g body wt) and maintained in artificial fresh water, calcium-rich fresh water, or calcium-deficient fresh water for 10 days. The specimens were sacrificed on Days 1, 3, 5, and 10 after initiation of the experiment. The blood samples were collected on these intervals and serum calcium and inorganic phosphate levels were analyzed. Vitamin D3 induced hypercalcemia and hyperphosphatemia in the freshwater catfish, H. fossilis. These effects of vitamin D3 are not dependent upon the calcium concentration of the different ambient media used in this study.

Animals↗
PubMed1992

Urine calcium and serum ionized calcium, total calcium and parathyroid hormone concentrations in the diagnosis of primary hyperparathyroidism and familial benign hypercalcaemia.

A relationship between serum concentrations of ionized calcium and parathyroid hormone (PTH) in persons without parathyroid overactivity was defined by performing an oral calcium load test. As a result, a serum PTH concentration greater than 2.6 pmol/L in a hypercalcaemic patient was regarded as suggestive of hyperparathyroidism. Fasting serum PTH concentrations in 58 patients with surgically and histologically proven primary hyperparathyroidism (PHPT) were all above 2.7 pmol/L (range 3.2-84.5). Thirteen of 20 patients with familial benign hypercalcaemia (FBH) had fasting serum PTH concentrations greater than 2.6 pmol/L (range 1.6-6.1). There was a significant correlation between serum PTH and age in the FBH patients only. Fasting urine calcium excretion (CaE) ranged from 14 to 222 mumol/L of glomerular filtrate in PHPT and 3-34 mumol/L of glomerular filtrate in FBH. The best biochemical discriminant between patients with PHPT and FBH was a plot of fasting serum PTH against CaE. A plot of post-calcium load PTH against post-load CaE showed no further significant advantage in discriminating between the two conditions.

Adolescent↗
PubMed1990

Osteoclast cytosolic calcium, regulated by voltage-gated calcium channels and extracellular calcium, controls podosome assembly and bone resorption.

The mechanisms of Ca2+ entry and their effects on cell function were investigated in cultured chicken osteoclasts and putative osteoclasts produced by fusion of mononuclear cell precursors. Voltage-gated Ca2+ channels (VGCC) were detected by the effects of membrane depolarization with K+, BAY K 8644, and dihydropyridine antagonists. K+ produced dose-dependent increases of cytosolic calcium ([Ca2+]i) in osteoclasts on glass coverslips. Half-maximal effects were achieved at 70 mM K+. The effects of K+ were completely inhibited by dihydropyridine derivative Ca2+ channel blocking agents. BAY K 8644 (5 X 10(-6) M), a VGCC agonist, stimulated Ca2+ entry which was inhibited by nicardipine. VGCCs were inactivated by the attachment of osteoclasts to bone, indicating a rapid phenotypic change in Ca2+ entry mechanisms associated with adhesion of osteoclasts to their resorption substrate. Increasing extracellular Ca2+ ([Ca2+]e) induced Ca2+ release from intracellular stores and Ca2+ influx. The Ca2+ release was blocked by dantrolene (10(-5) M), and the influx by La3+. The effects of [Ca2+]e on [Ca2+]i suggests the presence of a Ca2+ receptor on the osteoclast cell membrane that could be coupled to mechanisms regulating cell function. Expression of the [Ca2+]e effect on [Ca2+]i was similar in the presence or absence of bone matrix substrate. Each of the mechanisms producing increases in [Ca2+]i, (membrane depolarization, BAY K 8644, and [Ca2+]e) reduced expression of the osteoclast-specific adhesion structure, the podosome. The decrease in podosome expression was mirrored by a 50% decrease in bone resorptive activity. Thus, stimulated increases of osteoclast [Ca2+]i lead to cytoskeletal changes affecting cell adhesion and decreasing bone resorptive activity.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗