Platelet cytosolic free calcium concentration and parathyroid hormone: changing relationships with haemodialysis in end-stage renal disease

1992 ◽  
Vol 82 (6) ◽  
pp. 651-658 ◽  
Author(s):  
R. J. Fluck ◽  
A. C. McMahon ◽  
F. M. Alameddine ◽  
A. B. S. Dawnay ◽  
L. R. I. Baker ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Ionized Calcium ◽  
Free Calcium ◽  
Dialysis Session ◽  
Hormone Concentration ◽  
Serum Parathyroid Hormone ◽  
Cytosolic Calcium Concentration ◽  
End Stage

1. Twelve patients receiving haemodialysis for end-stage renal failure were studied at a single dialysis session. Platelet cytosolic calcium concentration, plasma ionized calcium concentration and serum parathyroid hormone concentration were measured before dialysis, mid-dialysis and 30 min after dialysis. 2. Plasma ionized calcium concentration increased towards dialysate calcium concentrations, falling insignificantly after cessation of dialysis. Serum parathyroid hormone concentration fell by 39% during dialysis, with incomplete recovery afterwards. There was no overall change in platelet cytosolic calcium concentration. 3. Patients were divided into two subgroups: low parathyroid hormone (serum parathyroid hormone concentration < 10 pmol/l) and high parathyroid hormone (serum parathyroid hormone concentration > 10 pmol/l). Before dialysis, values of platelet cytosolic calcium concentration or plasma ionized calcium concentration were not statistically different between the subgroups, but the platelet cytosolic calcium concentration was higher in the high-parathyroid hormone subgroup during and after dialysis. 4. Before haemodialysis there was a linear correlation between plasma ionized calcium concentration and platelet cytosolic calcium concentration, which disappeared during dialysis. In contrast, there was no relationship between serum parathyroid hormone concentration and platelet cytosolic calcium concentration before dialysis, but after dialysis a hyperbolic relationship was evident. 5. These results suggest that uraemic toxins may interfere with cytosolic calcium homoeostasis, allowing passive diffusion of extracellular calcium to influence the resting concentration, and that this effect is reversible by haemodialysis.

Angiotensin II causes sustained elevations in cytosolic calcium in glomerulosa cells

1988 ◽  
Vol 255 (3) ◽  
pp. E338-E346 ◽  
Author(s):  
R. E. Kramer
Keyword(s):  
Angiotensin Ii ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Cytosolic Calcium Concentration ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Glomerulosa Cells

Studies were conducted to examine the effects of angiotensin II on cytosolic free calcium concentration in bovine adrenal glomerulosa cells maintained in primary culture. The calcium indicator, fura-2, and discontinuous dual-wavelength fluorescence spectroscopy were used to measure cytosolic free calcium in superfused adherent cell monolayers. Basal cytosolic free calcium concentration was 63.7 +/- 3.3 nM. The threshold concentration for angiotensin II-stimulated increases in cytosolic calcium was 10(-14)-10(-13) M, and maximal elevation of cytosolic calcium was produced by 10(-9) M angiotensin II. Angiotensin II (10(-13) M) produced a gradual increase in cytosolic calcium concentration that plateaued after 3-5 min of superfusion at a level approximately 1.2 times that of control cells. The calcium signal invoked by a maximal concentration (10(-9) M) of angiotensin II, in contrast, was characterized by an immediate, intense (approximately 8-fold) increase in cytosolic calcium concentration that decayed within 5 min to a lower, but sustained, level 2.5-3 times that of control cells. The calcium signals invoked by intermediate concentrations (10(-12)-10(-10) M) of angiotensin II exhibited dose-dependent increases in magnitude and a gradual transition in nature between those invoked by threshold and maximal concentrations of the peptide. The effect of angiotensin II to increase cytosolic calcium concentration was accompanied by an increase in aldosterone output. The increase in steroidogenesis was most closely correlated with the magnitude of the initial calcium signal. At high concentrations (10(-10) and 10(-9) M) of angiotensin II, there was a clear dissociation between aldosterone output and the magnitude of the sustained calcium signal.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Calcium metabolism and cardiovascular function after spaceflight

2002 ◽  
Vol 92 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Daniel C. Hatton ◽  
Qi Yue ◽  
Jacqueline Dierickx ◽  
Chantal Roullet ◽  
Keiichi Otsuka ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Metabolism ◽  
Calcium Concentration ◽  
Dietary Calcium ◽  
Ionized Calcium ◽  
Free Calcium ◽  
Mineral Density ◽  
Spontaneously Hypertensive ◽  
Low Calcium ◽  
High Calcium

To determine the influence of dietary calcium on spaceflight-induced alterations in calcium metabolism and blood pressure (BP), 9-wk-old spontaneously hypertensive rats, fed either high- (2%) or low-calcium (0.02%) diets, were flown on an 18-day shuttle flight. On landing, flight animals had increased ionized calcium ( P < 0.001), elevated parathyroid hormone levels ( P < 0.001), reduced calcitonin levels ( P < 0.05), unchanged 1,25(OH)2D3levels, and elevated skull ( P < 0.01) and reduced femur bone mineral density. Basal and thrombin-stimulated platelet free calcium (intracellular calcium concentration) were also reduced ( P < 0.05). There was a tendency for indirect systolic BP to be reduced in conscious flight animals ( P = 0.057). However, mean arterial pressure was elevated ( P < 0.001) after anesthesia. Dietary calcium altered all aspects of calcium metabolism ( P < 0.001), as well as BP ( P < 0.001), but the only interaction with flight was a relatively greater increase in ionized calcium in flight animals fed low- compared with high-calcium diets ( P < 0.05). The results indicate that 1) flight-induced disruptions of calcium metabolism are relatively impervious to dietary calcium in the short term, 2) increased ionized calcium did not normalize low-calcium-induced elevations of BP, and 3) parathyroid hormone was paradoxically increased in the high-calcium-fed flight animals after landing.

A mathematical model of parathyroid hormone response to acute changes in plasma ionized calcium concentration in humans

2010 ◽  
Vol 226 (1) ◽  
pp. 46-57 ◽  
Author(s):  
Rajiv P. Shrestha ◽  
Christopher V. Hollot ◽  
Stuart R. Chipkin ◽  
Claus P. Schmitt ◽  
Yossi Chait
Keyword(s):  
Mathematical Model ◽  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Ionized Calcium ◽  
Hormone Response ◽  
Acute Changes

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

scholarly journals Protection against hydrogen peroxide cytotoxicity in Rat-1 fibroblasts provided by the oncoprotein Bcl-2: maintenance of calcium homoeostasis is secondary to the effect of Bcl-2 on cellular glutathione

1999 ◽  
Vol 340 (1) ◽  
pp. 291-297 ◽  
Author(s):  
Matthäus M. RIMPLER ◽  
Ursula RAUEN ◽  
Thorsten SCHMIDT ◽  
Tarik MÖRÖY ◽  
Herbert DE GROOT
Keyword(s):  
Cell Death ◽  
Calcium Concentration ◽  
Cell Injury ◽  
Cytosolic Calcium ◽  
Glutathione Metabolism ◽  
Transfected Cells ◽  
Cytosolic Calcium Concentration ◽  
Glutathione Status ◽  
Calcium Elevation ◽  
Reduced State

The oncoprotein Bcl-2 protects cells against apoptosis, but the exact molecular mechanism that underlies this function has not yet been identified. Studying H2O2-induced cell injury in Rat-1 fibroblast cells, we observed that Bcl-2 had a protective effect against the increase in cytosolic calcium concentration and subsequent cell death. Furthermore, overexpression of Bcl-2 resulted in an alteration of cellular glutathione status: the total amount of cellular glutathione was increased by about 60% and the redox potential of the cellular glutathione pool was maintained in a more reduced state during H2O2 exposure compared with non-Bcl-2-expressing controls. In our cytotoxicity model, disruption of cellular glutathione homoeostasis closely correlated with the pathological elevation of cytosolic calcium concentration. Stabilization of the glutathione pool by Bcl-2, N-acetylcysteine or glucose delayed the cytosolic calcium increase and subsequent cell death, whereas depletion of glutathione by DL-buthionine-(S,R)-sulphoximine, sensitized Bcl-2-transfected cells towards cytosolic calcium increase and cell death. We therefore suggest that the protection exerted by Bcl-2 against H2O2-induced cytosolic calcium elevation and subsequent cell death is secondary to its effect on the cellular glutathione metabolism.

TRAVELLING CALCIUM WAVES IN SYSTEMS WITH NON-DIFFUSING BUFFERS

2008 ◽  
Vol 18 (06) ◽  
pp. 883-912 ◽  
Author(s):  
BOGDAN KAZMIERCZAK ◽  
VITALY VOLPERT
Keyword(s):  
Structural Stability ◽  
Diffusion Coefficients ◽  
Calcium Concentration ◽  
Travelling Waves ◽  
Cytosolic Calcium ◽  
Calcium Waves ◽  
Cytosolic Calcium Concentration

The existence and structural stability of travelling waves of systems of the free cytosolic calcium concentration in the presence of immobile buffers are studied. The proof is carried out by passing to zero with the diffusion coefficients of buffers. Thus, its method is different from Ref. 13 where the existence is proved straightforwardly.

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