The acute hypocalcaemic effect of ethanol and its mechanism of action in the rat

1983 ◽  
Vol 61 (4) ◽  
pp. 388-394 ◽  
Author(s):  
Nateetip Krishnamra ◽  
Liangchai Limlomwongse
Keyword(s):  
Body Weight ◽  
Mechanism Of Action ◽  
Calcium Release ◽  
Calcium Influx ◽  
Plasma Calcium ◽  
In Vitro Studies ◽  
Calcium Efflux ◽  
Plasma Pool ◽  
Suppressive Action

The hypocalcaemic action of ethanol (3 g/kg body weight) was investigated in intact, thyroparathyroidectomized and antrectomized rats. It was found that ethanol administered either intraperitoneally or orally reduced plasma calcium concentrations within 30 min and that this response lasted for 8 h. Additional studies performed in antrectomized and thyroparathyroidectomized rats indicated that neither gastrin nor the hormones parathormone and calcitonin had any effect on the hypocalcaemic effect of ethanol. Investigation of the mechanism of action of ethanol-induced hypocalcaemia involved measurements of calcium efflux from and influx into the plasma pool. Ethanol did not have any effect on the disappearance from plasma of 45Ca administered intravenously at 0 min. In contrast, ethanol was found to enhance the disappearance of 45Ca administered intraperitoneally 17 h prior to the experiment. The interpretation of 45Ca studies was discussed and it was concluded that ethanol-induced hypocalcaemia resulted from a decrease in calcium influx into the plasma. Additional in vitro studies did not indicate the suppressive action of ethanol on the release of calcium from tibias. In conclusion, our results show that the mechanism of hypocalcaemia caused by ethanol is the suppression of calcium release from some tissue(s) into the plasma.

Effects of pH on bone calcium and proton fluxes in vitro

1983 ◽  
Vol 245 (2) ◽  
pp. F204-F209 ◽  
Author(s):  
D. A. Bushinsky ◽  
N. S. Krieger ◽  
D. I. Geisser ◽  
E. B. Grossman ◽  
F. L. Coe
Keyword(s):  
Alkaline Medium ◽  
Sodium Azide ◽  
Calcium Release ◽  
Calcium Influx ◽  
Calcium Flux ◽  
Metabolic Inhibitor ◽  
Calcium Efflux ◽  
Medium Ph ◽  
Proton Fluxes

Bone mineral is thought to decompose during acute and chronic metabolic acidosis and thereby contribute to buffering of the acid load. We cultured neonatal mouse calvariae for 3 h and found calcium efflux from bone when the medium pH was below 7.40, calcium influx into bone when the pH was above 7.40, and no net flux at pH 7.40. The calcium flux varied to the same extent when medium pH was altered by a primary change in the medium bicarbonate concentration or in the partial pressure of carbon dioxide. Calcium and proton fluxes were inversely correlated (r = -0.713, P less than 0.001), and the slope of the linear regression indicated that between 16 and 21 neq of proton entered the calvariae in exchange for each neq of calcium that left. In 24-h cultures, acid medium also caused net calcium efflux from bone, and alkaline medium caused net influx. PTH increased calcium efflux at acid but not at alkaline medium pH. Sodium azide resulted in net influx of calcium into bone at all values of medium pH. Calcium release by cultured calvariae in response to low medium pH is associated with proton buffering; over 3 h the stoichiometry indicates that little buffering is due to the dissolution of calcium-containing crystals. Effects of medium pH on calcium release are amplified by PTH, and calcium efflux can be prevented by the metabolic inhibitor sodium azide.

scholarly journals Network pharmacology-based analysis for unraveling potential cancer-related molecular targets of Egyptian propolis phytoconstituents accompanied with molecular docking and in vitro studies

RSC Advances ◽  
2021 ◽  
Vol 11 (19) ◽  
pp. 11610-11626
Author(s):  
Reham S. Ibrahim ◽  
Alaa A. El-Banna
Keyword(s):  
Molecular Docking ◽  
Cancer Treatment ◽  
Mechanism Of Action ◽  
Molecular Targets ◽  
Integrated Approach ◽  
In Vitro Studies ◽  
Network Pharmacology ◽  
Multi Level ◽  
Potential Cancer

Multi-level mechanism of action of propolis constituents in cancer treatment using an integrated approach of network pharmacology-based analysis, molecular docking and in vitro cytotoxicity testing.

Mechanism of proton-induced bone calcium release: calcium carbonate-dissolution

1987 ◽  
Vol 253 (5) ◽  
pp. F998-F1005 ◽  
Author(s):  
D. A. Bushinsky ◽  
R. J. Lechleider
Keyword(s):  
Metabolic Acidosis ◽  
Calcium Carbonate ◽  
Bone Mineral ◽  
Calcium Release ◽  
Calcium Efflux ◽  
Carbonate Phase ◽  
Bone Calcium ◽  
Calcium Carbonate Dissolution

Protons are buffered and calcium is released by bone during metabolic acidosis. Incubation of neonatal mouse calvariae in acid medium causes net calcium efflux from bone and net proton influx into bone, just as metabolic acidosis does in vivo. To determine whether the calcium carbonate phase of bone mineral is solubilized with increasing proton concentrations, we cultured calvariae for 3 h in medium in which the saturation was varied by changing pH or calcium and phosphate concentrations. We determined the driving force for crystallization by calculating the Gibbs free energy of formation (DG). With alteration of the medium pH, calcium carbonate entry or loss from bone varied linearly with the initial DG for medium calcium carbonate (r = -0.745, n = 41, P less than 0.001) as it did with alteration of the medium calcium and phosphate (r = -0.665, n = 118, P less than 0.001). There was dissolution of calcium carbonate into medium that was unsaturated with respect to calcium carbonate, net flux ceased at saturation, and calcium carbonate entered bone from supersaturated medium, indicating that the medium is in equilibrium with the calcium carbonate phase of bone mineral. Neither the mineral phase brushite nor apatite was in equilibrium with the medium. These observations indicate that in vitro, acute proton-induced calcium efflux is due to dissolution of bone calcium carbonate.

In Vitro Studies on the Environmental Biology of Goniodes Colchici (Denny) (Mallophaga:Ischnocera)

1971 ◽  
Vol 55 (2) ◽  
pp. 553-568
Author(s):  
R. T. WILLIAMS
Keyword(s):  
Body Weight ◽  
Water Vapour ◽  
Water Intake ◽  
The Body ◽  
In Vitro Studies ◽  
Normal Amount ◽  
Environmental Biology ◽  
Active Uptake ◽  
Survival And Reproduction

1. Active uptake of water vapour, following previous desiccation, has been studied in the pheasant body louse, Goniodes colchid (Denny). 2. Uptake is not continuous but occurs during limited periods of varying duration. 3. Water vapour is taken up by adult lice at temperatures of 32-44 °C and at humidities of 60-100 % R.H. The rate of uptake is not affected by temperature. The amount of uptake is not affected by humidity but is maximal at 36.8 °C. 4. Water vapour is not taken up at humidities below 50 % R.H. At 55 % R.H. about half of the lice take up the normal amount, the rest none at all. 5. Immature lice take up either much water vapour or none at all at temperatures of 32-44 °C; there is no temperature of maximal uptake. 6. Lice are unable to take up water vapour during moulting and/or starvation. But within 48 h of moulting they are often able to take up enough to increase the body weight above its pre-moult level. 7. It is concluded that in lice of this species the greater part of their water intake is by active uptake of water vapour. The conditions of temperature and humidity which these lice require for survival and reproduction can be understood on this basis.

In vitro studies on the mechanism of action of a new antiallergic, Ro 21-7634

1981 ◽  
Vol 11 (4) ◽  
pp. 345-351 ◽  
Author(s):  
Ann F. Welton ◽  
William C. Hope ◽  
Herman J. Crowley ◽  
Richard A. Salvador
Keyword(s):  
Mechanism Of Action ◽  
In Vitro Studies

scholarly journals Parathyroid hormone(1-34) and parathyroid hormone-related protein(1-34) stimulate calcium release from human syncytiotrophoblast basal membranes via a common receptor

2000 ◽  
Vol 166 (3) ◽  
pp. 689-695 ◽  
Author(s):  
W Farrugia ◽  
T de Gooyer ◽  
GE Rice ◽  
JM Moseley ◽  
ME Wlodek
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Release ◽  
Membrane Vesicles ◽  
Basal Membrane ◽  
Membrane System ◽  
Related Protein ◽  
Calcium Efflux ◽  
Parathyroid Hormone Related Protein ◽  
Pthrp Receptor

The placental syncytiotrophoblast is the site for mineral and nutrient exchange across the maternal-fetal interface. It has been proposed that parathyroid hormone-related protein (PTHrP) is a key factor in the maintenance of a maternal-fetal calcium gradient. Using simultaneously prepared microvillous (maternal facing) and basal (fetal facing) syncytiotrophoblast membranes from term human placentae (n=8), we determined the relative contribution of PTH(1-34), PTHrP(1-34) and PTHrP(67-94) to the regulation of syncytiotrophoblast calcium efflux. The vesicles had correct right-side-out membrane orientation and specific markers validated the fractionation of microvillous and basal membrane vesicles. Calcium efflux was studied by preloading vesicles with calcium-45 in the presence of calcium and magnesium and then incubating the vesicles at 37 degrees C for 15 min with the peptides. In basal membranes, PTHrP(1-! 34) significantly stimulated calcium efflux at a dose of 12.5 nmol/l, whereas PTH(1-34)-stimulated efflux was significant at 50 nmol/l (P<0.05, ANOVA). This efflux was significantly reduced in the presence of the PTH/PTHrP receptor antagonist (PTHrP(7-34)). Midmolecule PTHrP(67-94) had no significant effect on basal membrane calcium efflux. PTH(1-34), PTHrP(1-34) or PTHrP(67-94) had no significant effects on MVM calcium efflux. This study, using the human syncytiotrophoblast in vitro membrane system, demonstrated that PTHrP(1-34) and PTH(1-34) stimulate calcium transport across the basal, but not microvillous, syncytiotrophoblast membrane vesicles, mediated via the PTH/PTHrP receptor.

Enhanced vascular reactivity to various vasoconstrictor agents following pinealectomy in the rat: role of melatonin

1980 ◽  
Vol 58 (3) ◽  
pp. 287-293 ◽  
Author(s):  
Stephen C. Cunnane ◽  
Mehar S. Manku ◽  
Masatsugu Oka ◽  
David F. Horrobin
Keyword(s):  
Vascular Reactivity ◽  
Calcium Release ◽  
Calcium Influx ◽  
Extracellular Fluid ◽  
Heart Weight ◽  
Vasoconstrictor Agents ◽  
Vascular Responsiveness ◽  
Male Wistar Rats

The mesenteric vascular bed preparation of control and pinealectomized (PX) male Wistar rats was used to examine vascular reactivity to two concentrations each of norepinephrine, serotonin, angiotensin, and potassium. Vasoconstrictor responses to 50- and 100-ng injections of norepinephrine and 0.5- and 1.0-μg injections of serotonin were 30–40% higher in preparations from PX rats. Responses to 100 ng but not to 50 ng of angiotensin were also significantly higher in preparations from PX rats. Responses to 1.5- and to 3.0-mg injections of potassium did not differ significantly in either case. In vivo injection of 20 μg of melatonin 3 h prior to dissection of the preparation, or in vitro perfusion of 20 ng melatonin per millilitre of buffer completely reversed the increased vascular response to all vasoconstrictor agents tested in the PX preparations, but had little effect in control preparations. Also observed in PX rats was a significant increase in blood pressure, serum sodium, and increased body and heart weight. Arterial wall sodium was also elevated in PX rats. These changes may be relevant to the increased vascular reactivity of PX rats. The increased vascular responsiveness of PX rats may be specific for agents that stimulate calcium release from intracellular stores (norepinephrine, angiotensin) rather than those that stimulate calcium influx from extracellular fluid (potassium). Melatonin lack may be the cause of the vascular changes in the PX rats as both in vivo and in vitro it lowered the vasoconstrictor effects of the agents tested, but only in PX rats; it had no significant effect in the control rats.

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