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Results for “CALCIUM METABOLISM”

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At least 19 recordsLinked to original sources
PubMed1995

Calcium metabolism, calcium supplementation and hypertensive disorders of pregnancy.

In recent years growing attention has been directed towards the possible role of calcium in the development of pregnancy-induced hypertension and preeclampsia. Several studies describe calcium metabolism in normal and hypertensive pregnancy, but so far, they have shown discrepant and inconsistent results. Intracellular free calcium, which plays an important role in vascular smooth muscle contraction, has been claimed as a pathogenic factor in hypertensive disorders of pregnancy. Although there is discordance in the data, a possible role of intracellular calcium in the development of hypertensive disorders of pregnancy cannot be excluded. Observational studies in pregnant women suggest an inverse association between calcium intake and the incidence of hypertensive disorders of pregnancy. Despite large methodological differences, the results from the calcium supplementation trials support this finding. Although it is rather difficult to isolate the effect of calcium intake from the intake of other mineral elements, results from calcium supplementation trials are supportive for calcium being the most important. Proposed mechanisms by which calcium supplementation may lower blood pressure involve changes in parathyroid hormone (PTH) level, the renin-angiotensin system and calcium as a modifier of vascular agent regulation, but none of these have yet been elucidated. At present, circumstantial evidence suggest a positive role for calcium in the prevention of hypertensive disorders of pregnancy, but definite evidence is lacking and further research is warranted.

Calcium↗
PubMed1976

Erythrocyte calcium metabolism. Calcium exchange in normal and sickle-cell-anaemia erythrocytes.

Under exchange conditions (no net increase in calcium), erythrocytes incubated in isoosmotic phosphate-buffered saline have an exchangeable calcium pool comprising about 10% of the total erythrocyte calcium. This pool reaches exchange equilibrium, for either inward-directed or outward-directed transfer of the 45Ca-exchange label, with a half-time of about 20 min. The uptake of Ca2+ requires phosphate, even under hypo-osmotic conditions, where the calcium loading expected as the cells swell is obtained only when phosphate is present. The phosphate requirement is not due to Ca2+ transport as a phosphate salt. This exchangeable-calcium pool is also present in sickle-cell-anemia erythrocytes, and comprises a similar proportion of total cellular calcium.

Anemia, Sickle Cell↗
PubMed1993

Amphibian calcium metabolism.

Calcium is present in amphibian blood at a concentration similar to that in other vertebrates, about 1-2 mmol l-1. The fraction of free calcium in amphibians is lower than that in other tetrapod vertebrates because about 50% of the plasma Ca2+ is bound to plasma proteins and perhaps other molecules. Plasma [Ca2+] varies seasonally, increasing in spring and summer and decreasing in winter. Changes in plasma [Ca2+] also occur during larval development, as the concentration of this ion increases in larval forms as they approach metamorphosis. Calcium is exchanged at a variety of sites in animals. There is evidence for Ca2+ uptake across the skin and gills of larval anurans. It is also transported into the blood from the small intestine (especially the duodenum) and reabsorbed in renal tubules from the glomerular filtrate. The possibility of Ca2+ absorption from urine stored in the urinary bladder has not been confirmed, however. Calcium is stored in bone and in specialized endolymphatic sacs. This Ca2+ can be mobilized when the need arises. There are a number of endocrine and other humoral factors that appear to be involved in amphibian calcium metabolism. These include parathyroid hormone, calcitonin, vitamin D and prolactin.

Absorption↗
PubMed1988

Calcium metabolism, calcium-channel blocking agents, and hypertension management.

Increasing evidence has suggested that a disturbance of cellular calcium metabolism may have a role in initiating and maintaining elevated systemic vascular resistance in essential hypertension. Controversy exists over whether calcium can alleviate or exacerbate the hypertensive process, and diversity of calcium metabolism in hypertensive patients has been proposed. Calcium-channel blocking agents are potent vasodilators capable of correcting the elevated systemic vascular resistance. Clinical studies have shown that these drugs have antihypertensive efficacy comparable to established agents. The elderly, blacks, and patients with low renin activity respond well to calcium-channel blockers. These drugs may also offer potential advantages over established antihypertensive agents in patients with other coexisting diseases. Sustained release formulations have been developed, and initial experience with long-term efficacy and tolerability is encouraging. The calcium-channel blockers may become first-line therapy for treatment of hypertension in selected patients.

Calcium↗
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↗
PubMed2004

Bone markers, calcium metabolism, and calcium kinetics during extended-duration space flight on the mir space station.

UNLABELLED: Bone loss is a current limitation for long-term space exploration. Bone markers, calcitropic hormones, and calcium kinetics of crew members on space missions of 4-6 months were evaluated. Spaceflight-induced bone loss was associated with increased bone resorption and decreased calcium absorption. INTRODUCTION: Bone loss is a significant concern for the health of astronauts on long-duration missions. Defining the time course and mechanism of these changes will aid in developing means to counteract these losses during space flight and will have relevance for other clinical situations that impair weight-bearing activity. MATERIALS AND METHODS: We report here results from two studies conducted during the Shuttle-Mir Science Program. Study 1 was an evaluation of bone and calcium biochemical markers of 13 subjects before and after long-duration (4-6 months) space missions. In study 2, stable calcium isotopes were used to evaluate calcium metabolism in six subjects before, during, and after flight. Relationships between measures of bone turnover, biochemical markers, and calcium kinetics were examined. RESULTS: Pre- and postflight study results confirmed that, after landing, bone resorption was increased, as indicated by increases in urinary calcium (p < 0.05) and collagen cross-links (N-telopeptide, pyridinoline, and deoxypyridinoline were all increased >55% above preflight levels, p < 0.001). Parathyroid hormone and vitamin D metabolites were unchanged at landing. Biochemical markers of bone formation were unchanged at landing, but 2-3 weeks later, both bone-specific alkaline phosphatase and osteocalcin were significantly (p < 0.01) increased above preflight levels. In studies conducted during flight, bone resorption markers were also significantly higher than before flight. The calcium kinetic data also validated that bone resorption was increased during flight compared with preflight values (668 +/- 130 versus 427 +/- 153 mg/day; p < 0.001) and clearly documented that true intestinal calcium absorption was significantly lower during flight compared with preflight values (233 +/- 87 versus 460 +/- 47 mg/day; p < 0.01). Weightlessness had a detrimental effect on the balance in bone turnover such that the daily difference in calcium retention during flight compared with preflight values approached 300 mg/day (-234 +/- 102 versus 63 +/- 75 mg/day; p < 0.01). CONCLUSIONS: These bone marker and calcium kinetic studies indicated that the bone loss that occurs during space flight is a consequence of increased bone resorption and decreased intestinal calcium absorption.

Alkaline Phosphatase↗
PubMed1990

Growth hormone (replacement) therapy in adults: bone and calcium metabolism.

Calcium uptake from the gut is increased by GH effects on vitamin D metabolism or action. Bone metabolism is stimulated by many factors, of which GH and insulin-like growth factor I (IGF-I) are only two examples. From various animal and human data, it can be shown that GH and IGF-I seem to influence bone formation more than bone resorption. However, GH excess, as seen in acromegaly, does not result in increased bone mass. GH was used to treat osteoporosis in a few clinical trials. In only one, in combination with calcitonin, an increase in bone mass was observed. In GH-deficient adult patients, substitution therapy resulted in a temporary increase in serum calcium levels. Effects on bone mineral mass were only found in a pilot study performed by us in a group of 8 GH-deficient adult patients. The mean increase of bone mineral mass was 0.04 g hydroxyapatite/cm2, p less than 0.05. These data indicate that GH substitution can result in increased bone mass.

Bone and Bones↗
PubMed1995

Pathophysiology of calcium metabolism.

Calcium (Ca) is a mineral that plays a central role in maintaining the homeostasis of vertebrate animals, including muscle contraction, blood coagulation, enzyme activity, neural excitability, hormone secretion, and cell adhesion.(1) It is also involved in the pathogenesis of metabolic diseases which disrupt the normal regulation of Ca balance and may result in hypercalcemia or hypocalcemia.(2) The purpose of this manuscript is to review current concepts of the function of Ca, its regulation, and the role of Ca in specific disease processes.

Journal Article↗
PubMed1990

[Ionized calcium. An essential parameter for the study of calcium metabolism].

Calcium ions in plasma are either free (ionized calcium) or bound to protein and small anions. Ionized calcium is the physiologically active fraction. Several factors have recently been combined to change the measurement of ionized calcium from a specialized to a routine test. Reliable instrumentation, easy to maintain, is now available with simultaneous pH measurement. This paper focuses on both the analytical consideration required to perform reliable laboratory measurements and the clinical situations where ionized calcium has proved to provide a substantially different clinical interpretation than the measurement of total calcium.

Adolescent↗
PubMed1999

Disorders of maternal calcium metabolism implicated by abnormal calcium metabolism in the neonate.

Normal fetal and neonatal calcium homeostasis is dependent upon an adequate supply of calcium from maternal sources. Both maternal hypercalcemia and hypocalcemia can cause metabolic bone disease or disorders of calcium homeostasis in neonates. Maternal hypercalcemia can suppress fetal parathyroid function and cause neonatal hypocalcemia. Conversely, maternal hypocalcemia can stimulate fetal parathyroid tissue causing bone demineralization. We report two asymptomatic women, one with previously unrecognized hypoparathyroidism and the other with unrecognized familial benign hypercalcemia, who were diagnosed when their newborn infants presented with abnormalities of calcium metabolism. J.B. was born at 34 weeks' gestation with transient hyperbilirubinemia and thrombocytopenia. At 1 month of age he had severe bone demineralization, cortical irregularities, widening and cupping of the metaphyses, and lucent bands in the scapulae. The total serum calcium and phosphorus were normal with an ionized calcium of 5.4 mg/dL (4.6-5.4). His alkaline phosphatase, parathyroid hormone, and 1,25-dihydroxyvitamin D levels were all increased. P.B., mother of J.B., had no symptoms of hypocalcemia either prior to, or during this pregnancy. She had severe hypocalcemia and hyperphosphatemia, laboratory values typical of hypoparathyroidism. J.N. presented at 6 weeks of age with new onset of seizures and tetany secondary to severe hypocalcemia. The serum phosphorus, creatinine, alkaline phosphatase, and parathyroid hormone levels were normal. At 15 weeks of age his calcium was slightly elevated with a low fractional excretion of calcium. P.N., mother of J.N., had no symptoms of hypercalcemia either prior to, or during this pregnancy. Her serum calcium was 12.7 mg/dL and urine calcium was 66.5 mg/24 hr, with a low fractional excretion of calcium ranging from 0.0064 to 0.0073. P.N. has a brother who previously had parathyroid surgery. Both J.N. and P.N. meet the diagnostic criteria for familial benign hypercalcemia. These cases illustrate the important relationships between maternal serum calcium levels and neonatal calcium homeostasis. They emphasize the need to assess maternal calcium levels when infants are born with abnormal serum calcium levels or metabolic bone disease.

Adolescent↗
PubMed1991

Calcium metabolism and calcium requirements during skeletal modeling and consolidation of bone mass.

The degree of positive calcium balance in young individuals necessary to achieve peak bone mass and density is unknown. To assess calcium requirements and metabolism during acquisition of peak bone mass, 487 calcium balance studies from published reports were analyzed. The results suggest that 1) calcium intake and skeletal modeling and turnover determine calcium balance during growth, 2) the highest requirements for calcium are during infancy and adolescence and then during childhood and young adulthood, 3) to meet high calcium requirements, infants and adolescents have higher calcium absorption, 4) calcium absorption during rapid bone modeling and turnover is mediated by the Nicolaysen's endogenous factor, 5) urinary calcium reaches its maximum by the end of puberty, 6) calcium intake has little influence on urinary calcium excretion during the period of rapid growth, 7) the recommended dietary allowance for calcium should be higher than the amount currently established for children, adolescents, and young adults to ensure a level of skeletal retention of calcium for maximal peak bone mass, and 8) clinical trials with increased calcium intakes in each age segment of young populations are needed to clarify the above trends.

Absorption↗
PubMed1985

The effect of milk supplements on calcium metabolism, bone metabolism and calcium balance.

Twenty-two healthy postmenopausal women were divided into two groups, one group of 13 received milk supplementation of 24 oz per day and the other group of 9 controls received no intervention during two years of observation. Extensive inpatient metabolic balance and radiocalcium kinetic studies were performed at the beginning and at the end of one year of observation. In the milk supplement group, fractional calcium absorption (x +/- SD) decreased from .243 +/- .058 to .176 +/- .058, absorbed calcium increased from .159 +/- .052 gm/d to .248 +/- .063 gm/d, urine calcium increased from .117 +/- .034 gm/d to .146 +/- .027 gm/d, bone accretion decreased from .385 +/- .079 gm/d to .326 +/- .063 gm/d, bone resorption decreased from .446 +/- .098 gm/d to .342 +/- .106 gm/d and endogenous fecal calcium increased from .105 +/- .023 gm/d to .120 +/- .021 gm/d. All these changes were significant within the group and the mean changes were significantly different from the mean changes observed in the control group. Calcium balance in the milk supplemented group improved from -.061 +/- .056 gm/d to -.017 gm/d +/- .073 gm/d. Predicted changes in calcium and bone metabolism held true except that the suppression of bone remodeling was less than previously found using calcium carbonate supplements. We conclude that milk and milk products can be recommended as sources of calcium, that data on the effects of increasing calcium intake from other sources can be applied to milk and that milk may offer an advantage because it does not suppress bone remodeling as severely as calcium carbonate.

Aged↗