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At least 19 recordsLinked to original sources
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

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↗
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↗
PubMed1977

Dependence of ionophore- and caffeine-induced calcium release from sarcoplasmic reticulum vesicles on external and internal calcium ion concentrations.

The effects of the ionophore, X537A, and caffeine on ATP-dependent calcium transport by fragmented sarcoplasmic reticulum were studied in the absence (calcium storage) or presence (calcium uptake) of calcium-precipitating anions. The ionophore caused rapid calcium release after calcium storage, the final level of calcium storage being the same whether a given concentration of X537A was added prior to initiation of the reaction or after calcium storage had reached a steady state. Although 10 to 12 muM X537A caused approximately 90% inhibition of oxalate-supported calcium uptake when added prior to the start of the reaction, this ionophore concentration caused only a small calcium release when added after a calcium oxalate precipitate had formed within the vesicles, and only slight inhibition of calcium uptake velocity when added during the calcium uptake reaction. When low initial calcium loads limited calcium uptake to 0.4 mumol of calcium/mg of protein, subsequent calcium additions in the absence of the ionophore led to renewed calcium uptake. Uptake of the subsequent calcium additions was not significantly inhibited by 10 to 12 muM X537A. These phenomena are most readily understood in terms of constraints imposed by fixed Cai (calcium ion concentration inside the vesicles) on the pump-leak situation in sarcoplasmic reticulum vesicles containing a large amount of an insoluble calcium precipitate, where most of the calcium is within the vesicles and Cai is maintained at a relatively low level. These constraints restrict calcium loss after calcium permeability is increased because calcium release can end when the calcium pump is stimulated by the increased Cao (calcium concentration outside the vesicles) so as to compensate for the increased efflux rate. In contrast, an increased permeability in vesicles that have stored calcium in the absence of a calcium-precipitating ion causes a much larger portion of the internal calcium store to be released. Under these conditions calcium storage capacity is low so that release of stored calcium is less able to raise Cao to levels where the calcium pump can compensate for the increased efflux rate. The constraints imposed by anion-supported calcium uptake explain the finding that more calcium is released by X537A or caffeine when these agents are added at higher levels of Cao, and that more calcium leaves the vesicles in response to a given increase in calcium permeability at higher Cai. Although such calcium release is amplified by increased Cao, the amplification is attributable to the constraints described above and does not represent a "calcium-triggered calcium release."

Animals↗
PubMed1977

Studies on the mechanism of renin release from isolated superfused rat glomeruli: effects of calcium, calcium ionophore and lanthanum.

1. The effects of external medium calcium concentration, the ionophore A(23187) and lanthanum on the rate of renin release in vitro were studied with particular emphasis on results obtained from isolated superfused glomeruli of rat kidneys.2. The response to reduction in superfusate calcium concentration from 2 mM was a graded and reversible increase in the rate of renin release. An increase in release was detectable at 0.2 mM calcium; a threefold increase was found 36 min after a change from 2 mM calcium to calcium-free superfusate. A similar relative increase in release resulted from reductions from 0.1 mM to zero calcium, but the absolute amounts of renin released were greater in this latter series. Renin release from kidney cortical slices similarly increased in response to calcium-free incubation medium.3. The effects of A(23187) on renin release were modest. Changing from 2 mM calcium during control periods to calcium-free Ringer with A(23187) added caused an attenuated and more delayed increase in release than the change to calcium-free Ringer without ionophore. This difference in response was abolished when glomeruli were superfused with 0.1 mM calcium during the preceding 1 hr control period. There was no significant difference in renin release from glomeruli exposed to calcium-free EGTA-Ringer with and without A(23187) in the 2 mM calcium series; in the 0.1 mM calcium series the increase in release following a shift to calcium-free EGTA-containing superfusate with A(23187) added was significantly greater than in the absence of the ionophore.4. Addition of lanthanum (1 or 0.05 mM) to calcium-containing as well as calcium-free superfusate resulted in a significant depression of renin release. Subsequent removal of the lanthanum did not restore the rate of release unless EGTA was added; in the latter case a massive increase in renin release occurred resulting in a marked depletion of the remaining renin content of the glomeruli.5. It is concluded that calcium influences renin release by a direct action on the juxtaglomerular cells. The data support the previous suggestion that basal renin release is a function of active, calcium-dependent cell volume regulation - swelling causing an increase in the release; and further suggest that membrane-bound calcium has a direct effect on the cell membrane permeability to renin.6. The results exclude that calcium-stimulated exocytosis is responsible for basal renin release from the juxtaglomerular cells adhering to isolated glomeruli.

Animals↗
PubMed1977

Dependence of calcium permeability of sarcoplasmic reticulum vesicles on external and internal calcium ion concentrations.

The ability of sarcoplasmic reticulum vesicles to retain calcium following ATP-supported calcium uptake in the presence of the calcium-precipitating anions oxalate and phosphate depends on Cao (calcium ion concentration outside the vesicles) and Cai (calcium ion concentration within the vesicles). Calcium efflux rates at any level of Cai are accelerated when Cao is increased. Higher Cao at the time that calcium uptake reactions reach steady state is associated with a spontaneous calcium release that reflects this effect of increased Cao. Increasing Cai at any level of Cao causes little or no acceleration of calcium efflux rate so that calcium permeability coefficients, estimated by dividing calcium efflux rates by Cai, the "driving force", are inversely proportional to Cai. Calcium permability coefficients thus correlate, as a first approximation, with the ratio Cai/Cao, decreasing 1000-fold as this ratio increases over a 3000-fold range (Cao = 0.1 to 3.3 muM, Cai =4 to 750 muM). Oscillations in both the calcium content of the vesicles and Cao are seen as calcium uptake reactions approach steady state, suggesting that calcium permeability undergoes time-dependent variations. Sudden reduction of Cao to levels that markedly inhibit calcium influx via the calcium pump unmasks a calcium efflux that decreases slowly over 60 to 90 s. The maximal calcium permeability observed in the present study would allow the calcium efflux rate from the sarcoplasmic reticulum at a Cai of 100 muM to be approximately 10(-10) mol/cm2/s, which is about 1 order of magnitude less than that estimated for the sarcoplasmic reticulum of activated skeletal muscle in vivo. The release of most of the stored calcium in some experiments indicates that the observed permeability changes can occur over a large portion of the surface of the sarcoplasmic reticulum.

Animals↗
PubMed1979

Effects of dietary calcium on blood and tissue lipids, tissue phospholipids, calcium and magnesium levels in rabbits fed diets containing beef tallow.

Levels of lipids, calcium and magnesium in blood and tissue were examined in rabbits to determine the effects of 20% beef tallow diets containing three levels of calcium, less than 0.02, 0.8 or 1.6%. In plasma, the calcium-deficient (less than 0.02%) diet contributed to elevated cholesterol and phospholipid, but had no effect on triglyceride levels. Plasma calcium decreased in the calcium-deficient group and plasma magnesium decreased in the high-calcium (1.6%) group of rabbits. Lipid levels of some tissues varied with the level of dietary calcium. Cholesterol, total phospholipid, sphingomyelin and phosphatidylethanolamine were generally elevated in livers of calcium-deficient rabbits, but the individual phospholipids were decreased in skeletal muscle. Lungs of the calcium-deficient group also had lower phospholipid levels than the high-calcium group. Liver, kidneys, brain and adipose tissue triglyceride levels were highest in the high-calcium group. The calcium level of skeletal muscle was lower in the calcium-deficient group than in the high-calcium group. Calcium in brain and adipose tissue were highest in the calcium-deficient group. Except for adipose tissue, magnesium levels of the tissues studied were not affected by dietary calcium.

Animals↗
PubMed1979

Calcium requirement and calcium therapy.

The mean calcium requirement of normal adults has been estimated from 212 calcium balances on 84 normal subjects and found to be 578 mg. The calcium allowance required to ensure that 95% of normal adults are in calcium balance is about 900 mg. Calcium requirement is relatively higher than that of phosphorus or magnesium because plasma calcium--and therefore urine calcium--is maintained at the expense of the skeleton in the presence of calcium deficiency, whereas plasma phosphate and magnesium--and therefore urine phosphate and magnesium--fall on phosphorus and magnesium deficient diets. Calcium requirement appears to rise at the menopause, and postmenopausal bone loss can be reduced by calcium supplements. In postmenopausal osteoporosis, the severe negative calcium balance can be corrected by giving calcium or calcium and vitamin D, but vitamin D alone is not beneficial. Similarly, bone loss, height loss and further vertebral compression can be reduced by calcium or calcium and vitamin D but not by vitamin D alone.

Bone Diseases↗
PubMed1975

Regulation of cellular calcium metabolism and calcium transport by calcitonin.

Calcitonin was studied in isolated kidney cells and in isolated mitochondria. A concentration of 10 ng/ml of synthetic calcitonin increases the cellular accumulation of 45Ca and the total cell calcium. The mitochondrial pool is increased several-fold. Kinetic analysis of the data shows that although the total cellular exchangeable calcium pool is enlarged, calcium influx and efflux are significantly depressed by calcitonin. The absence of phosphate or the presence of inhibitors of mitochondrial calcium transport completely abolish the effects of the hormone. In isolated mitochondria, the hormone stimulates the active calcium uptake and depresses the extramitochondrial calcium activity. Calcitonin counteracts the effects of cyclic AMP which stimulates the release of calcium from mitochondria and increases the extramitochondrial calcium activity. These data indicate that cellular calcium homeostasis is controlled by the mitochondrial calcium turnover. They suggest that calcitomin regulates the cell calcium metabolism and inhibits the transcellular calcium transport by stimulating the rate of calcium uptake by mitochondria which depresses cytoplasmic calcium activity.

Animals↗
PubMed1977

Calcium in bile and calcium salts in gallstones.

In gallbladder and common duct bile from patients undergoing cholecystectomy, usually because of gallstones, calcium was found to exist in at least 2 forms. Ultrafiltration showed some calcium was bound to substances with a molecular weight greater than 10 000, and the chief binding agent is likely to be the mixed micelle. Bound calcium was significantly less in common duct bile than in bile from functioning gallbladders, but the amount of ultrafiltrable calcium was the same. Furthermore, ultrafiltrable calcium in gallbladder bile from patients with cholesterol or some calcium carbonate in their gallstones was almost constant for a range of total calcium concentrations of 2.40--9.70 mmol/l. Comparison of ultrafiltrable and total calcium values for the different types of stone-formers showed that the deposition of calcium carbonate in gallstones was not related to any calcium measurement made. However, the presence of calcium phosphate and/or calcium bilirubinate in gallstones could be related to a significant increase in ultrafiltrable calcium in gallbladder bile.

Bile↗
PubMed1979

Critical appraisal of oral calcium load test for indirect assessment of intestinal calcium absorption.

Two methods of oral calcium load or tolerance test for the indirect assessment of calcium absorption were compared. In 16 patients in whom the diagnosis of absorptive hypercalciuria was made independently, an exaggerated urinary total calcium excretion during four hours following calcium load, indicative of increased calcium absorption according to the method of Pak et al., was found in 15 patients. An abnormally high increment in urinary calcium during third and fourth hours post-calcium load, suggestive of enhanced calcium absorption by the criteria of Broadus et al., was encountered in 14 patients. However, an exaggerated urinary total calcium following calcium load was found in all 7 patients with renal hypercalciuria, whereas only 4 were shown to have an enhanced increment in calcium excretion. It is concluded that both methods are equally reliable in the detection of increased calcium absorption in absorptive hypercalciuria. However, the technique of Broadus et al. is probably superior to that of Pak et al. in the disclosure of increased calcium absorption in renal hypercalciuria.

Administration, Oral↗
PubMed1977

Regulation of intracellular calcium in chick embryo fibroblast: calcium uptake by the microsomal fraction.

The total membrane fraction of a chick embryo fibroblast (CEF) homogenate accumulates calcium in an energy-dependent manner. This activity can be dissociated into azide-sensitive and azide-insensitive components. The azide-sensitive component of calcium uptake is believed to represent mitochondrial calcium uptake. The azide-insensitive component of calcium uptake is enhanced by the presence of a calcium trapping agent such as oxalate, and cannot utilize, ADP, inorganic phosphate and a Krebs cycle substrate to support uptake. The distribution of the azide-insensitive calcium uptake in subcellular fractions suggests that this uptake occurs in other than mitochondrial membranes. The membranes most likely to contribute to the azide-insensitive component of calcium uptake are the endoplasmic reticulum and plasma membrane. A microsomal preparation from CEF cells is essentially devoid of the azide-sensitive calcium uptake activity. This microsomal activity is similar in characteristics to the sarcoplasmic reticulum of skeletal muscle. However the specific activity of CEF microsomal calcium uptake system is much less than that found in the skeletal muscle system. The transport of calcium by these membranes provide a mechanism for the regulation of cytosol calcium levels and may play a role in the control of movement and growth of cultured cells.

Adenosine Diphosphate↗
PubMed1979

Effect of age on intestinal calcium absorption and adaptation to dietary calcium.

To study the reported decline in intestinal calcium absorption with age, calcium active transport, immunoreactive calcium protein (CaBP) content, and alkaline phosphatase activity were measured in the intestine of two strains of rats aged 3-wk--20 mo. Calcium active transport, as measured by everted gut sacs from Sprague-Dawley rats, was greatest at 3 wk, but it declined rapidly with no active transport demonstrable at 3 mo or thereafter. CaBP content closely paralleled the decline in active transport, but alkaline phosphatase activity increased as active transport decreased. Intestinal adaptation to dietary calcium was studied by feeding high- and low-calcium diets to Fischer 344 rats aged 1.5--12 mo. In 1.5-mo-old rats fed a low-calcium diet, there was an increase in calcium active transport, CaBP content, and alkaline phosphatase activity relative to animals fed a high-calcium diet. However, the magnitude of this intestinal adaptation decreased with age until there was only marginal adaptation by 12 mo. The observed changes in calcium active transport with age and diet may be explained by the parallel changes in the vitamin D-dependent CaBP content of the intestine.

Aging↗
PubMed1975

Low plasma ionized calcium and response to calcium therapy in critically ill man.

Marked lowering of plasma ionized calcium concentrations [Ca++] occurred in eight patients (2 days to 54 years old) who required extensive pharmacologic support of the circulation. [Ca++]'s ranged from 0.21 to 0.53 mM. Only one patient survived. The hypocalcemia occurred in the absence of massive transfusion of citrated whole blood or well after such transfusions had been discontinued. These abnormally low concentrations of ionized calcium were not readily corrected by intravenous administration of calcium salts in doses generally recommended. The process responsible for inadequate hemodynamic function appeared to be associated with a severe disturbance in calcium metabolism. Contribution of the latter to the severity of hemodynamic deterioration is unclear, and little benefit from intravenous calcium therapy was found. In two patients, normal [Ca++] could not be restored by administration of CaCl2 alone, but [Ca++] rose to normal following continued calcium replacement therapy in conjunction with increased isoproterenol infusion. There was no predictable relationship between total and ionized plasma calcium concentrations. Thus, measurement of total calcium provided no indication of the level of the biologically active moiety. [Ca++] was low with both normal and low plasma pH values. The data suggest that a very high infusion rate of CaCl2 may required to restore [Ca++] to normal and that hypocalcemia occurring during low-flow states often cannot be corrected by calcium therapy alone. It is recommended that calcium replacement therapy be undertaken only with close monitoring of [Ca++].

Adolescent↗