Changes In Plasma Calcium Concentration Research Articles

Calcium mobilisation following shell damage in the Pacific oyster, Crassostrea gigas

Shell growth of oysters requires calcium uptake from the environment and transport to the area of shell formation. A shell regeneration assay in combination with radiolabelled calcium was used to investigate uptake and distribution of calcium to different tissues and hemolymph fractions in Pacific oysters, Crassostrea gigas (Bivalvia, Ostreoida). Oysters were notched at the shell margin and subsequently sampled for hemolymph and grading of shell regeneration during a two week experimental period. Half of the oysters were additionally exposed to 45Ca and sampled for hemolymph and tissues. Total plasma calcium concentrations increased in notched oysters compared to controls on 1, 2 and 7days after notching. A decrease in plasma calcium levels was apparent on day 4, for both total and ionic calcium. The shell regeneration assay in the notched oysters resulted in a visible deposition of CaCO3 onto the regenerate from day 7 onwards. This was coinciding with an increased uptake of total calcium on days 11 and 14 as well as free, i.e. ionic and ligand-bound calcium, on day 14. At day 1, notching also increased calcium uptake into the mantle tissues, in areas above the notch and near the hinge. During the experiment, both the total hemocyte count and the number of granulocytes increased in notched compared to control oysters. The present study suggests that induced shell damage results in a dynamic regulation of the calcium uptake from the environment and the distribution of calcium within the body, starting directly after notching. Increases in both total calcium concentrations and uptake rates coincided with the visible depositions of CaCO3 on the regenerate shell. C. gigas was found to transport calcium mainly in the ionic form in the hemolymph, with only minor parts being bound to proteins or smaller ligands. Hemolymph measurement also revealed that C. gigas is able to regulate the extracellular concentrations of calcium and potassium. The changes in plasma calcium concentrations and speciation, concomitant with increases in granulocytes indicate that multiple calcium transport processes are activated after induced shell damage.

Fine structure of thyroid gland in wild caught female bat Taphozous kachhensis (Dobson) during reproductive cycle

The thyroid gland has long been recognized as an important modulator of reproductive function. Both hyper- and hypo-thyroidism are associated with reproductive dysfunction and infertility. In addition, thyroid hormones appear to play a key role in the expression of events that underlie seasonal reproductive cycles. Despite the considerable information is available on the histology of thyroid gland in some of the bats, literature related to study is very few, and further information available on the ultrastructure is also scanty. The specimen of Taphozous kachhensis was collected from Ambai Nimbi. Many collections were made during the breeding season so as to coincide with the time of reproductive cycle and to get an accurate pregnancy record. Thyroid is removed from the bat and cut into 1–2mm piece and immersed in fresh ice-cold 3% gluteraldehyde solution for 2–4h and send for further process. The thyroid gland is more active during estrus than the pregnancy and lactation. The cell organelles observed in follicular cell of thyroid gland indicate more synthetic activity. While during pregnancy and lactation the thyroid gland is not synthetically active but the appearance of more lysosomal bodies during pregnancy indicate the utilization of stored colloid and release of thyroid hormone in blood stream. The parafollicular cells are more developed during pregnancy and lactation than estrus as indicated by ultrastructural characteristics. These cells may secrete calcitonin, serotonin, and somatostatin and may be responsible for controlling the seasonal changes in plasma calcium concentration in this bat.

Dose response to vaginal administration of 1,25-dihydroxyvitamin D 3 to cows

It was previously reported that intravaginal (IVAG) administration of 1,25-dihydroxyvitamin D 3 (1,25(OH) 2D 3) might be protective against bovine hypocalcaemia. In the present study, various doses of exogenous 1,25(OH) 2D 3 were administered IVAG to ovariectomised cows, and the subsequent changes in the biochemical parameters of the blood were measured to assess the characteristics of vaginal absorption. Five cows received 1,25(OH) 2D 3 IVAG at a dose of 0.125, 0.25, 0.5, or 1.0 μg/kg of body weight (BW) or intravenously at a dose of 1.0 μg/kg BW. Dosing was at intervals of at least two weeks in a 5 × 5 Latin square design. Vaginally administered 1,25(OH) 2D 3 was absorbed in a dose-dependent manner. There was no correlation between the IVAG dose of 1,25(OH) 2D 3 and subsequent changes in plasma calcium concentrations. The bioavailability of 1,25(OH) 2D 3 administered IVAG at 1.0 μg/kg BW was approximately 93%.

Changes in plasma-calcium concentration following subtotal thyroidectomy.

Changes in plasma-calcium concentration following subtotal thyroidectomy.

Dietary calcium and health

Dietary calcium and health

Separate effects of 1,25-dihydroxyvitamin D and calcium on renal calbindin-D28k and intestinal calbindin-D9k.

The effects of normal, low and high plasma concentrations of 1,25-(OH)2vitamin D (1,25-(OH)2D) combined with normal, low and high concentrations of plasma calcium on renal calbindin-D28k and intestinal calbindin-D9k were examined in rats. We found that the expression of renal calbindin-D28k was significantly (P<0.05) increased by high levels of 1,25-(OH)2D, but was not affected by a 50% reduction in 1,25-(OH)2D. In contrast the intestinal calbindin-D9k responded significantly (P<0.005) to both high and low 1,25-(OH)2D levels. The effect of 1,25-(OH)2D on intestinal calbindin-D9k was modulated by plasma calcium concentrations. Increased plasma calcium levels did not affect the renal calbindin-D28k concentrations, but suppressed intestinal calbindin-D9k (P<0.05). The effect of calcium was not mediated by calciotropic hormones. This suggests the existence of a calcium-sensing mechanism in the proximal duodenum. It is concluded that intestinal calbindin-D9k is more sensitive than renal calbindin-D28k to changes in 1,25-(OH)2D and that intestinal calbindin-D9k in contrast to renal calbindin-D28k is sensitive to changes in plasma calcium concentrations.

Calcium intake by rats: influence of parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D.

We examined the contribution of the primary hormones of calcium homeostasis to the control of calcium intake in the rat. Male Sprague-Dawley rats with 50 mM CaCl2 solution as their only source of calcium received subcutaneous hormone infusions for 13 days. Parathyroid hormone (PTH; 40, 80, or 160 ng/h) produced sustained dose-related decreases in CaCl2 intake. High doses of calcitonin (CT; 32 or 64 ng/h) increased CaCl2 intake transiently, and low doses (4, 8, or 16 ng/h) had no effect. 1,25-Dihydroxyvitamin D [1,25(OH)2D] in doses > 1 ng/h initially increased CaCl2 intake, but the effects of moderate doses (2 or 4 ng/h) tended to dissipate, and the sustained effect of high doses (8 or 16 ng/h) was to reduce CaCl2 intake. Infusions of combinations of the hormones had effects consistent with their individual actions: there was no evidence for synergy. Based on changes in plasma hormone concentrations, it appeared that most of the infusions had effects within the physiological range. Consistent with hypotheses that calcium appetite is mediated by circulating calcium, PTH and CT infusions produced reciprocal changes in plasma calcium concentrations and CaCl2 intake. However, the finding that 1,25(OH)2D elevated both plasma calcium concentrations and CaCl2 intake raises the possibility that one or more of the hormones may mediate calcium appetite directly.

G-Protein-Coupled, Extracellular Ca2+-Sensing Receptor: A Versatile Regulator of Diverse Cellular Functions

Publisher Summary This chapter examines the importance of G-protein-coupled, extracellular Ca 2+ -sensing receptor as a versatile regulator of diverse cellular functions. In the extracellular space, calcium is a cofactor for clotting factors, adhesion molecules, and other proteins. It also regulates neuronal excitability and is an essential component of the mineral phase of the skeleton. Bone provides both a structural framework protecting crucial bodily structures and enabling locomotion and a large reservoir of mineral ions that can be mobilized in times of need. The maintenance of near constancy of Ca 2+ in tetrapods necessitates that specific cells of the mineral ion homeostatic system detect and respond in a homeostatically appropriate manner to the changes in plasma calcium concentration of the same order as its normal variability. Elevated levels of Ca 2+ also stimulate several aspects of osteoblast function in vitro that could promote increased bone formation in vivo and, therefore, reductions in Ca 2+ . The evidence for the presence of a G-protein-coupled CaR came from studies in bovine parathyroid cells examining the actions of Ca 2+ , the physiological agonist for the putative CaR, on intracellular second messengers. A variety of polyvalent cations mimic the actions of Ca 2+ on the osteoclast, but their pharmacological profile in this cell type differs distinctly from that in parathyroid and other CaR-expressing cells.

Calcium regulation in vertebrates: An overview

All cells maintain the calcium concentration of their cytoplasm below that of the surrounding fluids. In resting eucaryotic cells the cytoplasmic calcium activity is less than 1 /*M and although there have been no direct measurements in procaryotes, indirect evidence suggests that here too it may be less than 1 PM (Ordal, 1977). Why should Ca2+ be maintained at such a low concentration m all cells? The answer may ultimately derive from the very low solubility of calcium phosphates in water. The phosphatedominated energy economy of cells is of very ancient origin and, at neutral pH, is incompatible with high concentrations of calcium (Kretsinger, 1977). The maintenance of a low intracellular calcium concentration must, therefore, have long been of paramount importance. Cells have the capacity to regulate their internal calcium concentration and, in many cases, they can restore it to normal after periods of rapid calcium entry. It, therefore, seems unlikely that the resting cytoplasmic calcium activity would be directly affected by modest changes in the calcium concentration of extracellular fluids. Nevertheless, it is unclear to what extent precise intracellular calcium homeostasis is dependent on a stable extracellular calcium concentration (Bronner, 1982). In mammals, even small changes in plasma calcium concentration can be deleterious. Hypocalcaemia, for example, causes neuromuscular hyperexcitabihty which seems to result from an extracellular effect of calcium on membrane resistance (Frankenhaeuser and Hodgkin, 1957). Changes in extracellular calcium concentration also substantially affect the responses of cells to agonists that gate calcium, for example, glucosestimulated insulin release from pancreatic islets (Curry et al., 1968). Although the resting cell may be able to regulate its cytoplasmic calcium activity despite changes in plasma calcium, the extracellular and second messenger functions of calcium require that the plasma calcium concentration is stable. For some marine invertebrates that stability is provided by a

Delirium tremens and related clinical states: changes in calcium and inorganic phosphate concentrations in plasma and cerebrospinal fluid.

Calcium and inorganic phosphate were measured in blood and cerebrospinal fluid (CSF) in 11 patients during impending delirium tremens (grade 2) and in nine patients with fully developed delirium tremens (grade 3). The initial sampling of blood and CSF was performed at admission before treatment was initiated. The blood sampling was repeated daily until recovery and at this time a second lumbar puncture was also performed. In grade 3 patients the plasma calcium concentration showed a transient increase after admission; in grade 2 patients the plasma calcium concentration was also somewhat elevated. The changes in plasma calcium concentration after admission correlated significantly with the changes in blood alcohol concentration. In grade 3 patients the CSF calcium concentration decreased between admission and recovery, this possibly relating to an increased cerebral binding capacity in the post intoxication period. No statistically significant changes were seen in either of the diagnostic categories as far as plasma inorganic phosphate concentrations are concerned. CSF inorganic phosphate concentration decreased in a fashion correlated with CSF alcohol concentration and, finally, CSF inorganic phosphate at admission was somewhat lower in grade 3 patients as compared to grade 2, this possibly reflecting a more severe disturbance of cerebral metabolism in grade 3 patients. Essentially, grade 3 patients had lower CSF concentrations of both calcium and inorganic phosphate as compared to grade 2 patients and thus there may exist real differences in the metabolism of these two ions when a severe withdrawal reaction (grade 2) is compared to fully developed delirium tremens (grade 3).

15 Effect of Small Changes in Plasma Calcium Concentration on Responsiveness of Forearm Resistance Vessels in Normal Subjects

15 Effect of Small Changes in Plasma Calcium Concentration on Responsiveness of Forearm Resistance Vessels in Normal Subjects

Plasma aspirin esterases in normal individuals, patients with alcoholic liver disease and rheumatoid arthritis: characterization and the importance of the enzymic components.

Abstract. Two enzymes in human plasma capable of hydrolysing aspirin (‘aspirin esterases’) were isolated (by ion exchange and gel chromatography) and characterized, since their activity has been reported to be important in certain disease/therapeutic situations. The optimum pH and calcium concentration for plasma aspirin esterases were 80 and 5 mmol/1 respectively.The main enzymic activity (enzyme ‘C’) was associated with plasma cholinesterases. This component had a Km of 6‐5 mmol/1 for aspirin and a Kmax of 0–27 /imol salicylate/mg protein/min at pH 80 (Ca2+ present). It was not acetylated by aspirin but was inhibited by anti‐cholinesterase agents (eserine, echothiophate) and the neuromuscular blocking agent, decameth‐onium. The other enzymic component in plasma was albumin esterase.The sex difference in aspirin esterase activity in normal individuals previously reported by Menguy and co‐workers [1] was re‐investigated since it appeared that they had employed non‐optimal assay conditions. No significant differences were observed between the sexes in either normal individuals or patients with rheumatoid arthritis when the enzyme was assayed at either pH 7‐4 or the optimal pH of 80 (with Ca2+ added). The plasma albumin esterase activity was, however, markedly depressed in patients with alcoholic liver cirrhosis when assayed at pH 7‐4 and 80. Plasma aspirin esterases were elevated in nine rheumatoid arthritic patients receiving gold salt or D(‐)penicil‐lamine. Aspirin esterase 'C activity was negatively correlated with pain score in the plasma of female but not male rheumatoid arthritics. Also the percentage activation by calcium of aspirin esterase was correlated with the concentration of plasma calcium indicating that small changes in plasma calcium concentration may markedly affect enzymic activity.These results suggest that certain drugs (anti‐cholinesterase agents), disease states (e.g. alcoholic liver cirrhosis) or genetic deficiences (e.g. inactive pseudo‐cholinesterase) may be potentially important in the pharmacological and iatrogenic activities of aspirin.

Radioimmunoassay of calcitonin in the plasma of rhesus monkey and man.

We describe a radioimmunoassay for rhesus monkey and human immunoreactive calcitonin, in which a selected goat anti-human calcitonin antiserum, 131I-labeled synthetic human calcitonin tracer, and purified synthetic human calcitonin standards were used. The mean basal concentration of calcitonin in normal monkey plasma (254 microgram/liter) was not significantly different from that in normal human plasma (217 microgram/liter). The data indicate that the method is sensitive (lower limit of detection, 5 ng/liter), specific, accurate, and reproducible (coefficient of variation, 1-11% over a wide range of concentrations). Monkey calcitonin response to changes in plasma calcium concentration is similar to that in man, with significant correlation between calcium and calcitonin concentrations. Use of this radioimmunoassay for monkey and human calcitonin allows the monkey to be used in further studies of factors regulating secretion, function, and metabolism of calcitonin under various experimental conditions that would not be feasible in man.

RAPID CALCIUM INFUSION TEST FOR HYPERPARATHYROIDISM. FURTHER EXPERIENCES.

The normal response to calcium infusion is a decreased urinary phosphate excretion, presumably as a result of inhibition of parathyroid hormone secretion by the induced hypercalcemia. 1-3 In contrast, such a change in phosphaturia does not occur in the presence of hyperparathyroidism, and it has been suggested that the hyperfunctioning parathyroid tissue is absolutely or relatively autonomous, and hence unresponsive to changes in plasma calcium concentration. 1 We have reported previously 4,5 the efficacy of a simple diagnostic test for hyperparathyroidism which takes advantage of this differential response to calcium infusion. Both normal subjects and patients with hyperparathyroidism exhibit a progressively increasing phosphaturia between the hours of 8AMand 12 noon. The rapid infusion of calcium at 9AMprofoundly alters this phosphaturic rhythm in normal subjects, but has little or no effect upon the rhythm in patients with hyperparathyroidism. However, we have observed some limitations and potential sources

Changes in Plasma Calcium Concentration During Egg Formation

ABSTRACT DURING egg formation, large quantities of calcium are deposited as carbonate on the developing shell. The site of shell formation, the oviduct shell gland, is not a calcium storage organ; consequently, calcium must be mobilized rapidly from body stores to meet the periodic requirements of shell formation. Since the body calcium is located almost entirely in osseous tissue, it must pass through the circulatory system in rather large quantities during each period of active shell formation (about 14 hours; Bradfield, 1951). There is also an increase in calcium absorption from the gut during shell formation (Buckner et al., 1930), which contributes to the fluctuation in blood calcium concentration. The literature contains several reports of the influence of shell formation on blood calcium. Charles and Hogben (1933) found that plasma calcium concentration during egg formation was about 20% higher than during non-laying periods. However, their data for hens with a forming . . .