Reduction In Uptake Of Calcium Research Articles

Derangement of calcium metabolism in diabetes mellitus: negative outcome from the synergy between impaired bone turnover and intestinal calcium absorption.

Both types 1 and 2 diabetes mellitus (T1DM and T2DM) are associated with profound deterioration of calcium and bone metabolism, partly from impaired intestinal calcium absorption, leading to a reduction in calcium uptake into the body. T1DM is associated with low bone mineral density (BMD) and osteoporosis, whereas the skeletal changes in T2DM are variable, ranging from normal to increased and to decreased BMD. However, both types of DM eventually compromise bone quality through production of advanced glycation end products and misalignment of collagen fibrils (so-called matrix failure), thereby culminating in a reduction of bone strength. The underlying cellular mechanisms (cellular failure) are related to suppression of osteoblast-induced bone formation and bone calcium accretion, as well as to enhancement of osteoclast-induced bone resorption. Several other T2DM-related pathophysiological changes, e.g., osteoblast insulin resistance, impaired productions of osteogenic growth factors (particularly insulin-like growth factor 1 and bone morphogenetic proteins), overproduction of pro-inflammatory cytokines, hyperglycemia, and dyslipidemia, also aggravate diabetic osteopathy. In the kidney, DM and the resultant hyperglycemia lead to calciuresis and hypercalciuria in both humans and rodents. Furthermore, DM causes deranged functions of endocrine factors related to mineral metabolism, e.g., parathyroid hormone, 1,25-dihydroxyvitamin D3, and fibroblast growth factor-23. Despite the wealth of information regarding impaired bone remodeling in DM, the long-lasting effects of DM on calcium metabolism in young growing individuals, pregnant women, and neonates born to women with gestational DM have received scant attention, and their underlying mechanisms are almost unknown and worth exploring.

Sequential homo‐interpenetrating polymer networks of poly(2‐hydroxyethyl methacrylate): Synthesis, characterization, and calcium uptake

AbstractFormation of homo‐interpenetrating polymer networks (homo‐IPNs) of poly(2‐hydroxyethyl methacrylate) (PHEMA) and their capacity for calcification are investigated. A sequential method is established to generate IPNs of rank I and II, containing two or three crosslinked networks. Although the networks are chemically identical, thermo‐mechanical analysis (DSC, DMA) suggests some phase separation. Calcification of PHEMA hydrogels, thought to be controlled by the free volume pathways accessible to calcium ions, is investigated by positron annihilation lifetime spectroscopy (PALS) and experimental calcium deposition. While calcium uptake is reduced in IPNs, the size of the free volume elements estimated by PALS remain constant at radii of 2.6 Å (dry) and 2.9 Å (hydrated), both in PHEMA and IPNs. The reduction of calcium uptake cannot be therefore associated with the size reduction of the angstrom‐size free volume elements detectable by PALS, and is attributed to the effect of chain packing on pores too large to be detected by PALS. © 2012 Wiley Periodicals, Inc. J Appl Polym Sci, 2012

Effect of Redundant Chain Packing on the Uptake of Calcium Phosphate in Poly(2-Hydroxyethyl Methacrylate) Hydrogels

A method is described that allows reduction of the amount of calcium phosphate phases deposited spontaneously inside poly(2-hydroxyethyl methacrylate) (PHEMA), a hydrogel of biomedical importance. PHEMA homo-interpenetrating polymer networks (homo-IPNs) were synthesized and then treated in a calcifying solution. A reduction of calcium uptake of 58 to 75% was measured by ICP emission spectroscopy in the IPNs as compared to the PHEMA homopolymer (the parent network). The effect was rationalized in terms of reduction of the free volume available for the penetration and transport of Ca2+ and phosphate ions as a result of redundant chain packing through formation of IPNs.

The influence of chronic verapamil treatment on calcium absorption and homeostasis in the geriatric rat

It has been demonstrated that verapamil produces a significant reduction in calcium transport in rat everted gut sacs in vitro. The purpose of the present study was to determine the effect of oral verapamil treatment on calcium absorption and homeostasis in vivo in the geriatric rat. Verapamil was administered (either oral or parenteral) to groups of 12-month-old female rats at a moderate (5 mg/kg) to large (15 mg/kg) dose over a period of 8 weeks. At the end of the 8-week treatment period, calcium transport was examined in duodenal segments and femoral bone was removed to measure bone density and mechanical strength. Blood levels of verapamil as measured by high pressure liquid chromatography were consistent with the administered dose. The results of this study indicate that chronic verapamil treatment at a dose of 15 mg/kg caused an increase in calcium transport, a reduction in calcium uptake into duodenal tissue, and an increase in serum and urinary calcium. Therefore, these results support the concept that chronic oral and/or parenteral use of calcium channel blocking agents may alter calcium homeostasis in the geriatric patient.

Cardiovascular Protective Properties of Indapamide

Although indapamide has been used for many years as a first-line treatment of hypertension, it is only recently that some of its activities on the changes of the cardiovascular system, brought on by age and high blood pressure, have been studied. Indapamide appears to reduce blood pressure by a combined diuretic and direct vascular activity reducing vascular reactivity and total peripheral resistance. In addition, it has discrete effects on a number of interrelated systems that may protect the cardiovascular system. Indapamide reduces intracellular calcium levels, maintains magnesium ions, but reduces phosphate ions that may be involved in arterial rigidity. Circulating catecholamines remain unchanged but there is a reduction in normetanephrine, suggesting a reduction in sympathetic tone. It stimulates prostacyclin synthesis, increases levels of circulating prostacyclin, reduces platelet aggregation and stimulates the vasodilation elicited by endothelium-derived relaxing factor in the presence of bradykinin. In addition, it inhibits the formation of the vasoconstrictor prostanoid, thromboxane A 2. The free radical scavenging activity of indapamide could also protect the vascular smooth muscle from the reperfusion injury of cerebral and myocardial ischemia. Indapamide induces a reduction in cerebral ischemia after carotid ligation. Unlike some other antihypertensives, it does not upset the high-density/low-density lipoproteincholesterol balance, reducing the possible risk of atherosclerosis. Moreover, the combination of binding to elastin and reduction in uptake of calcium and phosphate into the smooth muscle could be a mechanism for reducing arterial rigidity seen in the elderly and hypertensive patient. In hypertensive patients, these properties induce an improvement in arterial compliance, and in the long term a reduction in left ventricular hypertrophy. These pharmacologic and clinical results, together with a good antihypertensive efficacy and acceptability, suggest that indapamide may be a preferential agent in the long-term cardiovascular protection of the hypertensive patient.

Barbiturate reduction of calcium-dependent action potentials: Correlation with anesthetic action

Calcium-dependent action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture following addition of the potassium channel blockers tetraethylammonium ion and 3-aminopyridine. The pharmacologically active barbiturates, pentobarbital and phenobarbital, but not the pharmacologically inactive barbiturate, barbituric acid, produced reversible, dose-dependent reduction of action potential duration at sedative-hypnotic and anesthetic concentrations. Pentobarbital reduced action potential duration at concentrations from 25 to 600 μM (50% reduction at 170 μM) while phenobarbital reduced action potential duration at concentrations from 100 to 5000 μM (50% reduction at 900 μM). The barbiturate concentrations which reduced calcium-dependent action potential duration in this study correlate with reduction of neurotransmitter release from other neuronal preparations and with reduction of calcium uptake by synaptosomes. The results suggest that barbiturates may produce anesthesia in part by reduction of presynaptic calcium entry and consequent reduction of neurotransmitter release in addition to postsynaptic increase of membrane chloride ion conductance. Barbiturate anticonvulsant actions are probably due to postsynaptic augmentation of GABA-mediated inhibition and depression of excitatory synaptic transmission. The major difference between anticonvulsant (phenobarbital) and anesthetic (pentobarbital) barbiturates was the dose-dependency of these actions. Phenobarbital produced postsynaptic modulation of neurotransmitter responses at low concentrations and decreased calcium-dependent action potential duration and increased chloride ion conductance at high concentrations. In contrast, pentobarbital produced all actions at low concentrations. Thus for phenobarbital there would be a large therapeutic index for anticonvulsant activity compared to anesthetic activity but for pentobarbital there would be a small therapeutic index.

Some observations on the ecology, metal uptake and nickel tolerance of Alyssum serpyllifolium subspecies from the Iberian peninsula

Experiments were carried out on the tolerance to, and uptake of, nickel by three iberian subspecies of Alyssum serpylliforium Desf. Two of these subspecies, the serpentine-endemic ssp. lusitanicum from Braganca, Portugal and ssp. malacitanum from Malaga, Spain, are hyperaccumulators (> 1000 μg/g in dried material) of nickel. Their possible ancestor, ssp. serpyllifolium (from Granada, Spain) was a non-accumulator of this element. Seeds of the two serpentine-endemics germinated extensively in nickel concentrations up to 12 000 μg/g (1.2%) whereas ssp. serpyllifolium only germinated in nickel concentrations below 60 μg/ml. Tolerance tests involving measurement of new root lengths of excised seedlings placed in varying nickel concentrations, again showed much greater tolerance of the two serpentinophytes. In both series of experiments, the order of tolerance was: ssp. lusitanicum > ssp. malacitanum > ssp. serpyllifolium. In pot trials involving seedlings of ssp. malacitanum grown in mixtures containing varying amounts of calcium, magnesium, and nickel, the most important finding was that plants will tolerate higher nickel contents in the soil when excess calcium is added. This is achieved by lowering the uptake of nickel. There appeared to be some concomitant reduction in calcium uptake in the presence of nickel, and some increase in uptake of magnesium. The resultant lower calcium/magnesium ratio in the plant, though not symptomatic of a favourable condition for colonization of serpentine soils, probably results from a mechanism which renders nickel innocuous to the plant at the expense of calcium uptake. It is suggested that the physiological characters of ssp. lusitanicum and ssp malacitanum are sufficiently different to support arguments for promoting the latter to full specific rank as has now been done for ssp. lusitanicum.

An effect of estradiol and testosterone on the calcium pump activity and phospholipid fatty acid composition of rat liver microsomes.

Castration of the male rat resulted in a 28% reduction of the specific activity of liver microsomal calcium uptake, three weeks after castration. Treatment of the castrated animals with testosterone during this period returned calcium uptake to control levels. Treatment with estradiol resulted in a reduction of calcium uptake to a level less than 25% of that seen in the normal male. Although testosterone treatment had only a small effect on the fatty acid composition of liver microsomal phospholipids in the castrated male, there were significant changes of linoleic acid (18:2) in phosphatidylcholines and of palmitic acid (16:0) in phosphatidylethanolamines, when compared to the untreated castrated male rat. Administration of estradiol to the castrated male rat resulted in a marked decrease of palmitic acid (16.0) and linoleic acid (18.2) in all three phospholipid fractions studied. Stearic acid (18.0) was significantly increased in the phosphatidylcholines and phosphatidylethanolamines by estradiol treatment. The phospholipid and calcium uptake changes seen after treatment of the castrated rat with testosterone or estradiol are consistent with the sex-related differences observed in the intact, adult rat liver microsomes.