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PubMed2002

[Therapeutic agents for hyperphosphatemia].

Hyperphosphatemia is one of the major causes of secondary hyperparathyroidism (II degrees HPT) in dialysis patients. Aluminum (Al) hydroxide was commonly used as a phosphate binder in Japan until the beginning of the 1990's, when it was replaced by calcium(Ca) compounds to eliminate undesirable side effects. Although Ca compounds are effective phosphate binders, the concomitant use of vitamin D derivatives can often result in hypercalcemia. For the reason, physicians today have been requesting phosphate binders that contain neither Al nor Ca. In this paper, we introduce several such phosphate binders. Sevelamer hydrocholoride (SH) is a new phosphate binder that contains neither Al nor Ca, and is not absorbed from the gastrointestinal tract. Several short-term clinical studies have established that SH is as efficient as calcium carbonate at lowering serum phosphorus (P) levels, with significant improvement in the Ca x P product and lipids metabolism. Furthermore, a long-term (52 weeks) study revealed that SH attenuated the progression of coronary and aortic calcification in hemodialysis (HD) patients. SH is considered a highly effective phosphate binder in protecting against the progression of II degrees HPT and cardiovascular death in HD patients.

English Abstract↗

PubMed1996

Using mineral trioxide aggregate as a pulp-capping material.

This study examined the dental pulp responses in monkeys to mineral trioxide aggregate, or MTA, and a calcium hydroxide preparation when used as pulp-capping materials. After the pulps of 12 mandibular incisors were exposed with a No. 1 round bur, they were capped with either MTA or the calcium hydroxide preparation. After five months, the authors noted no pulpal inflammation in five of six samples capped with MTA, and all six pulps in this group had a complete dentin bridge. In contrast, all of the pulps capped with the calcium hydroxide preparation showed pulpal inflammation, and bridge formation occurred in only two samples. Based on these results, it appears that MTA has the potential to be used as a pulp-capping material during vital pulp therapy.

Aluminum Compounds↗

PubMed1995

Interactions between angiotensin II and norepinephrine on renin release by juxtaglomerular cells.

While the interactions between angiotensin II (Ang II) and norepinephrine (NE) on cardiovascular responses are well known, their effects on renin responses are not. We determined the renin secretion rate (RSR) and intracellular calcium level in juxtaglomerular cells harvested from Sprague-Dawley rats using a radioimmunoassay and a two-dimensional calcium analyzer. The effect of Ang II and NE was inhibitory on RSR and stimulatory on intracellular calcium. The NE-induced RSR response was amplified in the presence of Ang II (20 nmol/l). The NE-induced intracellular calcium response was also potentiated by the Ang II. There was a significant correlation (r = 0.994, p < 0.0001) between the changes in the RSR and those in intracellular calcium levels. Losartan (0.1 mumol/l). an Ang II type 1 receptor antagonist, blocked the Ang II threshold RSR responses and completely abolished the Ang II-related enhancements. The exclusion of calcium from the buffer reduced the maximal RSR response to NE but did not prevent the enhancement, suggesting the importance of the mobilization of intracellular calcium in the mechanism. The Ang II-induced RSR was amplified in the presence of NE (0.2 mumol/l). The Ang II-induced intracellular calcium response was also potentiated by the NE. A significant correlation (r = 0.996, p < 0.0001) between the changes in the RSR and the changes in intracellular calcium levels was also noted. Prazosin (1 mumol/l), an alpha 1-adrenoceptor antagonist, blocked the NE threshold RSR responses and abolished the agonist-related enhancements. The calcium-free buffer diminished this amplication with a slight decrease in the maximum RSR response to Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2006

Effects of Ca2+ channel blockers on store-operated Ca2+ channel currents of Kupffer cells after hepatic ischemia/reperfusion injury in rats.

AIM: To study the effects of hepatic ischemia/reperfusion (I/R) injury on store-operated calcium channel (SOC) currents (I(SOC)) in freshly isolated rat Kupffer cells, and the effects of Ca(2+) channel blockers, 2-aminoethoxydiphenyl borate (2-APB), SK and F96365, econazole and miconazole, on I(SOC) in isolated rat Kupffer cells after hepatic I/R injury. METHODS: The model of rat hepatic I/R injury was established. Whole-cell patch-clamp techniques were performed to investigate the effects of 2-APB, SK and F96365, econazole and miconazole on I(SOC) in isolated rat Kupffer cells after hepatic I /R injury. RESULTS: I/R injury significantly increased I(SOC) from -80.4 +/- 25.2pA to -159.5 +/- 34.5pA ((b)P < 0.01, n = 30). 2-APB (20, 40, 60, 80, 100 micromol/L), SK and F96365 (5, 10, 20, 40, 50 micromol/L), econazole (0.1, 0.3, 1, 3, 10 micromol/L) and miconazole (0.1, 0.3, 1, 3, 10 micromol/L) inhibited I(SOC) in a concentration-dependent manner with IC50 of 37.41 micromol/L (n = 8), 5.89 micromol/L (n = 11), 0.21 micromol/L (n = 13), and 0.28 micromol/L (n = 10). The peak value of I(SOC) in the I-V relationship was decreased by the blockers in different concentrations, but the reverse potential of I(SOC) was not transformed. CONCLUSION: SOC is the main channel for the influx of Ca(2+) during hepatic I/R injuries. Calcium channel blockers, 2-APB, SK and F96365, econazole and miconazole, have obviously protective effects on I/R injury, probably by inhibiting I(SOC) in Kupffer cells and preventing the activation of Kupffer cells.

Animals↗

PubMed1990

[The anti-arrhythmia activity of isoteolin (IST)].

The antiarrhythmic activity of IST was studied on some experimental models of cardiac arrhythmia--caused by adrenaline in rats, caused by barium in non-narcotized rabbits, caused by strophanthin in guinea pigs, caused by aconitine and calcium in rats. Rhythmic disturbances were recorded by a 12-channel polyphysiograph "Galileo" or a single-channel electrocardiograph "Cardiomat". The obtained results showed that IST manifested antiarrhythmic activity in respect to adrenaline, barium and strophanthin arrhythmias without affecting substantially aconitine and calcium arrhythmias. It is thought that antiarrhythmic activity of IST, found in the indicated experimental models of cardiac arrhythmias, is most probably connected with a lowering of the peripheral sympathetic activity, realized by a central way.

Aconitine↗

PubMed1999

The effects of 2-aminoethoxydiphenyl borate, a novel inositol 1,4, 5-trisphosphate receptor modulator on myometrial contractions.

These studies were performed to evaluate the effect of 2-aminoethoxydiphenyl borate (2-APB), a novel membrane-permeable inositol 1,4,5-trisphosphate-receptor inhibitor on agonist-induced, spontaneous, and KCl-stimulated in vitro myometrial contractions. 2-APB significantly inhibited spontaneous myometrial contractions as well as phasic contractions induced by various uterotonic agonists. Confiriming its effects on intracellular calcium release, 2-APB inhibited phasic contractions in the absence of extracellular calcium. 2-APB had little effect on the tonic response to KCl stimulation, implicating its insignificant effect on voltage-gated calcium channels. The inhibitory effect of 2-APB on phasic contractions was completely reversed by washout. In summary, 2-APB effectively penetrated uterine tissue and significantly inhibited myometrial events previously shown to be mediated through activation of the PI-signaling pathway.

Animals↗

PubMed1990

[Reaction products of sevoflurane with new soda lime-A under various conditions].

Sevoflurane is reported to react with sodalime, a common carbon dioxide absorber which resolves into several products. We measured the reaction products of sevoflurane when this anesthetic reacted with sodalime-A, a new carbon dioxide absorber under various conditions. Analysis of reaction products was done by gas chromatography using a 2 m column packed with DOP. Six peaks including sevoflurane were detected on the gas chromatogram of sevoflurane after reaction with sodalime-A and five reaction products were obtained. These peaks were from P1 with the shortest retention time to P5 with the longest retention time. When sevoflurane was sealed with sodalime-A in a test tube at room temperature, 40 degrees C and 45 degrees C, only P1 was detected and two reaction products of P3 and P5 were identified when the test tube was heated at 50 degrees C. Sodalime contains Ca(OH)2, NaOH, KOH and silicon dioxide, and sodalime-A contains Ca(OH)2 and NaOH only. We reported previously that sevoflurane reacted with KOH to produce P1 to P5 even at room temperature and KOH was the most contributing factor to produce these reaction compounds. Reaction products of sevoflurane with two types of carbon dioxide absorber were checked with gas chromatography. Degradation products except P1 with sodalime-A was less than with conventional sodalime at any conditions. P1 production was about twice to three times more than that with sodalime.

Anesthetics↗

PubMed1999

AT1 calcium signaling in renal vascular smooth muscle cells.

Experiments were conducted to gain insight into calcium signaling mechanisms triggered by angiotensin II (AngII) stimulation in vascular smooth muscle cells (SMC) freshly isolated from preglomerular vessels of normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Cytosolic calcium concentration ([Ca2+]i) was measured using ratiometric Fura-2 fluorescence and a microscope-based photometer. Vascular SMC from preglomerular vessels were isolated and dispersed using an iron oxide-sieving method combined with collagenase treatment. AngII produced rapid increases in [Ca2+]i that remained elevated for the duration of continued stimulation. The same pattern of time response was observed in WKY and in SHR. AngII elicited dose-dependent increases in [Ca2+]i in groups of individual preglomerular arteriolar SMC from both strains. AngII (10(-10) M) induced an increase from baseline levels in WKY and SHR (37+/-9 and 32+/-13 nM; P < 0.05). In response to 10(-6) M AngII, steady-state responses were 165+/-30 and 170+/-35 nM (P < 0.01). The responses did not differ between strains (P > 0.4). The effects of AngII were inhibited by 88% by the AT1 receptor blocker candesartan in renal SMC. In SMC pretreated with calcium-free medium, baseline [Ca2+]i fell by about 60 nM. Thereafter, AngII did not elicit any [Ca2+]i response either in WKY or in SHR when calcium entry was prevented. Also, after prestimulation by AngII, a calcium-free solution completely reversed the effects of AngII. This study shows that AngII acts through AT1 receptors to stimulate [Ca2+]i by a predominant action on calcium entry with no evidence for calcium mobilization. Other studies have demonstrated that calcium entry in these SMC is mediated by voltage-gated, L-type entry channels sensitive to dihydropyridine agents. No strain differences were noted between the actions of AngII on individual renal SMC from SHR and normotensive control animals.

Angiotensin II↗

PubMed2007

Limited plasticity of mesenchymal stem cells cocultured with adult cardiomyocytes.

In order to assess, in a controlled in vitro model, the differentiation potential of adult bone marrow derived stem cells we have developed a coculture procedure using adult rat cardiomyocytes and mesenchymal stem cells (MSCs) from transgenic GFP positive rats. We investigated in the cocultured MSCs the time course of cellular processes that are difficult to monitor in in vivo experiments. Adult rat cardiomyocytes and adult rat MSCs were cocultured for up to 7 days and analyzed by confocal microscopy. Several markers were studied by immunofluorescence technique. The fluorescent ST-BODIPY-Dihydropyridine was used to label calcium channels in living cells. Intracellular calcium was monitored with the fluorescent probe X-Rhod-1. Immunofluorescence experiments showed the presence of connexin-43 between cardiomyocytes and MSCs and between MSCs, while no sarcomeric structures were observed at any time of the coculture. We looked at the expression of calcium channels and development of voltage-dependent calcium signaling in cocultured MSCs. MSCs showed a time-dependent increase of labeling of ST-BODIPY-Dihydropyridine, reaching a relatively strong level after 72 h of coculture. The treatment with a non-fluorescent DHP, Nifedipine, completely abolished ST-BODIPY labeling. We investigated whether depolarization could modulate intracellular calcium. Depolarization-induced calcium transients increased in MSCs in relation to the coculture time. We conclude that MSCs cocultured with adult cardiomyocytes present preliminary evidence of voltage-dependent calcium modulation uncoupled with the development of nascent or adult myofibrils, thus showing a limited lineage specification and a low plasticity to differentiate in a full cardiomyocyte-like phenotype.

Actinin↗

PubMed1989

Do differences in innervation result in different post-synaptic responses to exogenous agonists?

1. The pharmacological reactivity of the epididymal and prostatic portions of the rat vas deferens to BaCl2, phenylephrine and carbachol were recorded by isometric and isotonic technique. 2. The maximum response induced by the three agonists were similar at the epidiymal end, while at the prostatic portion phenylephrine produced a response 80% lower than that of barium and carbachol. 3. The pD2 value to agonists and the sensitivity to calcium channel blockers were lower at the prostatic end. 4. The data suggest that not only the pharmacological reactivity of the prostatic and epididymal portions differs, but also that the activity of the prostatic portion is much more reduced to alpha 1-agonists.

Animals↗

PubMed2000

Change of calcium and cAMP concentration by adrenoceptor agents in cultured porcine corneal endothelial cells.

It has been reported that beta-adrenergic receptors are localized in the corneal endothelial cells. In this study, the change of cellular signal transduction, such as intracellular calcium and cAMP, was determined with pure adrenergic agonists and commercial antiglaucoma adrenergic agents. The intracellular calcium of cultured porcine corneal endothelial cells was inhibited by 10 microM isoproterenol and norepinephrine, but enhanced by propranolol and 50 mM KCl. In the case of phenylephrine, calcium mobility did not alter significantly. Verapamil, at 10 microM, decreased intracellular calcium concentration. In the presence of isoproterenol, cellular cAMP concentration increased from 28.8 pmole/mg protein (1 microM) to 42.2 pmole/mg protein (100 microM) compared with control of 6.07 pmole/mg protein. Incubation with commercial adrenergic eye drops, such as betaxolol, caused the cAMP concentration to increase from 21.6 pmole/mg protein (0.0005%) to 39.1 pmole/mg protein (0.05%). Adding commercial levobunolol and timolol into cells caused cellular cAMP to increase from 14.3 pmole/mg protein (0.0005%) to 840.5 pmole/mg protein (0.05%) and from 115.2 pmole/mg protein (0.00025%) to 931.0 pmole/mg protein (0.025%), respectively. However, the preservative, benzalkonium chloride, increased cellular cAMP from 15.4 pmole/mg protein (0.00001 mg/ml) to 1087.4 pmole/mg protein (0.01 mg/ml). It is concluded that the intracellular calcium of corneal endothelium decreases when the cellular adrenergic receptor is activated by agonists. Benzalkonium chloride, due to its preservative in commercial antiglaucoma agents which increases cellular cAMP, may alter corneal endothelial physiology through long-term use.

Adrenergic Agonists↗

PubMed1992

Characterization of proton extrusion in sunflower cell cultures.

Cell suspensions derived from callus root tips of sunflower (Helianthus annuus L., cv. enano) were obtained in order to assess the effects of different chemical and physical agents on cell H+ extrusion. Cell H+ efflux was sensitive to temperature, pH, inhibitors of plasmalemma H(+)-ATPase and Ca2+ and K+ concentrations in the assay medium, as well as to the light intensity at which cells were cultivated. Thus, in the darkness and at 60 mumol/m2/s of illumination, a strong inhibition of H+ extrusion was detected as compared to cells grown at 30 mumol/m2/s. H+ extrusion by cells grown at 30 mumol/m2/s was unaffected by the presence of calcium in the assay medium, while at 60 mumol/m2/s such an activity increased when calcium was removed. These results provide the basis for the use of cell suspensions as an appropriate model to investigate the involvement of membrane-associated processes in plant tolerance mechanisms to different environmental stresses.

2,4-Dichlorophenoxyacetic Acid↗

PubMed2005

2-Aminoethoxydiphenyl borate perturbs hormone-sensitive calcium stores and blocks store-operated calcium influx pathways independent of cytoskeletal disruption in human A549 lung cancer cells.

Recent studies have identified novel actions for 2-aminoethoxydiphenyl borate (2-APB) in triggering calcium release and enhancing calcium influx induced by the depletion of intracellular calcium stores. In this study, we have examined the effects of 2-APB on the human lung adenocarcinoma A549 cell line, which we have previously shown displays a unique calcium influx response, when ER calcium stores are depleted by thapsigargin (TG) treatment. Here, we show that low concentrations of 2-APB failed to induce the rapid augmentation of TG-activated calcium influx previously reported for other cell types. We observed that store-operated calcium (SOC) channels in the A549 cell line exhibited short-term sensitivity to low doses of 2-APB, perhaps reflecting a delayed augmentation of SOC channel activity or the recruitment of 2-APB-insensitive SOC channels. In both intact and permeabilized cells, 2-APB effectively discharged a subset of A549 calcium pools corresponding to the hormone-sensitive intracellular calcium stores. The 2-APB-induced calcium release produced a long-lasting perturbation of the adenosine triphosphate (ATP)-releasable calcium pools, effectively uncoupling ATP-activated calcium release even, when stores are replenished with calcium. In contrast to previous reports, we found that disruption of either the actin or microtubule-based cytoskeleton failed to block the 2-APB-induced effects on calcium signaling in A549 cells. Our study describes novel cytoskeletal-independent effects of 2-APB on Ca2+-signaling pathways, revealing differentially sensitive Ca2+-influx pathways and long-term perturbation of hormone-sensitive Ca2+ stores.

Actins↗

PubMed2003

Lead bismuth calcium sodium phosphate: Pb4.6Bi0.4Ca2.6Na2.4(PO4)6.

The title compound, lead bismuth calcium sodium phosphate, Pb(4.6)Bi(0.4)Ca(2.6)Na(2.4)(PO(4))(6) crystallizes in the apatite structure type, with vacancies in sites 2a or 2b that are normally occupied by anions. The fact that the Bi and Pb ions are mainly localized in the 6h sites confirms the electron lone-pair influence on the apatite structure.

Journal Article↗

PubMed2003

MTA apexification combined with conventional root canal retreatment.

Apexification aims to induce apical closure of the open root apex with a hard-tissue barrier, against which a root filling can be compacted. Despite the popularity of the apexification procedure, calcium hydroxide therapy has some disadvantages that include variability of treatment time, unpredictability of apical closure, difficulties with patient follow-up and delayed treatment. Mineral trioxide aggregate (MTA) is a potential apical barrier material with good sealability and a high degree of biocompatibility. This paper demonstrates the placement of an apical barrier using MTA as an alternative to conventional long-term calcium hydroxide therapy.

Adolescent↗

PubMed2005

[Evaluation of the crystal inhibitory effect of angiotensin II type I receptor blocker in etylene glycol treated rat kidney].

PURPOSE: We examined whether there would be any inhibitive effect to the crystal formation in ethylene glycol treated rat kidney by angiotensin II type I receptor blocker (candesartan). METHODS: We divided 10-weeks-old male Sprague-Dawley rats into 4 groups. In these groups, rats were given tap water (group A), 1.0% ethylene glycol (group B), 1.0% ethylene glycol and 20 microg/ml candesartan (group C), 20 microg/ml candesartan (group D) for 4 weeks. Immunohistochemical studies of a renal tissue was performed by ED1 antibody and the osteopontin antibody, the transcription of renin, angiotensin converting enzyme, angiotensin II and osteopontin mRNA in whole kidney was determined using real time PCR and malondialdehyde level was measured. Renal tissue was evaluated using H.E. stain for counting the calcium deposit in the renal tubules. Calcium concentrations in whole kidney were measured with an atomic absorption spectrophotometer. RESULTS: Although there is no significant difference urinary oxalate and calcium levels compared with group B and C, group C showed fewer the numbers of calcium deposit in the tubules and decreased the amount of calcium contained in the whole kidney, ED1 positive cells, osteopontine mRNA expression and malondialdehyde level. CONCLUSION: These results suggest that candesartan inhibited superfluously induced osteopontin in the whole kidney by ethylene glycol and crystal formation was also related decreased.

Angiotensin II Type 1 Receptor Blockers↗

PubMed1983

Repeated I. V. injections of calcium salts give rise to increased exocrine pancreatic cell sensitivity to caerulein and urecholine in the dog.

The persisting modifications induced by repeated intravenous infusion of calcium salts were investigated in five dogs with Thomas fistulae. Five control dogs were also tested. In calcium treated dogs the pancreatic secretion stimulated by graded doses of either caerulein or urecholine showed: a) an increase in the sensitivity of acinar cells to caerulein and urecholine and potentiation by caerulein of the water and bicarbonate response to secretin, in contrast to the decreased sensitivity to secretin alone reported previously. b) an inhibition of water and bicarbonate secretion with urecholine stimulation, c) an inhibition of calcium secretion which was significant with caerulein. These findings could explain the data previously observed on basal pancreatic secretion of calcium treated dogs such as protein hypersecretion with protein precipitates and reduced bicarbonate secretion which are similar to modifications observed in chronic alcoholic dogs and men. These results have a clinical relevance to the understanding of the pathology of chronic pancreatitis.

Animals↗

PubMed1977

Sodium sensitive active transport of bretylium into adrenergic neurons for the development of blockade in rabbit ileum.

Transport of bretylium into adrenergic neurons was studied, using rabbit isolated periarterial nerve ileum preparations, by determining the effects of various incubation procedures, which inhibit noradrenaline uptake, to prevent or reverse the blockade. Adrenergic neuron blockade by bretylium 5 X 10(-5) (g/ml) was prevented but not reversed by incubation with sodium free and low temperature (10 degrees C) media. Ouabain 2.2 X 10(-8) and anoxia prevented bretylium-induced blockade. Noradrenaline 5 X 10(-6) and 8 X 10(-5) prevented and also reversed the blockade, but the reversing effect was transient. High calcium (totally 10 mM) readily reversed the bretylium-induced blockade, the recovery being complete and long-lasting. In light of the results, a sodium sensitive active transport of bretylium into adrenergic neurons is apparently necessary for development of adrenergic neuron blocking action in rabbit ilea.

Animals↗