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151.
Summary MC9 mast cells, sensitized with monoclonal IgE antibody specific for 2,4-dinitrophenyl (DNP) group, were exposed to DNP-BSA and the pH and cytosolic calcium signals were recorded by using the fluorescent probes BCECF and Fura-2 respectively. DNP-BSA induced cell alkalinization was fully inhibited by azelastine with IC50 (1.6±0.5 mol/l, mean±SEM, n = 5) similar to that required to inhibit histamine release (1.4 mol/l), Conversely, high azelastine concentrations (> 100 mol/l) were required to inhibit DNP-BSA-dependent cell calcium mobilization (IC50200 mol/l, n = 3). Amiloride, but not the H1 histamine antagonist pyrilamine, was able to inhibit the DNP-BSA induced pH signal. In acidified mast cells, azelastine potently inhibited Na+:H+ exchange activity (IC50 = 7.7±3.6 × 10–6 M, mean±SEM, n = 3). Conversely, in mouse spleen lymphocytes azelastine was unable to inhibit the amiloride-sensitive pH signal induced by concanavalin A. In conclusion, the inhibition of histamine release by azelastine is not due to an interference with the cytosolic calcium signal. Conversely, azelastine potently antagonized the allergen-dependent Na+: H+ exchange activation, suggesting an action on the protein kinase C signaling pathway.
Correspondence to: R. P. Garay at the above address 相似文献
152.
J. Y. Reginster D. Denis V. Bartsch R. Deroisy B. Zegels P. Franchimont 《Osteoporosis international》1993,3(5):271-275
Calcium (Ca) supplements have positive effects in growing children, reduce bone loss in late-postmenopausal women with a low calcium diet and, in association with vitamin D3 supplements, may reduce non-vertebral fracture rates in elderly women. However, for many formulated pharmaceutical products their relative beneficial effects have not been conclusively established. We have compared the acute (6 h) metabolic responses following oral administration of two preparations of calcium gluconolactate and carbonate (CG and CG), tricalcium phosphate (TCP) and calcium citrate (CC), given on separate occasions in each of 10 healthy young male volunteers. The subjects fasted overnight for 12 h and continued to fast during the experimental procedure. A 1000 mg dose of each Ca salt was ingested at weekly intervals. Blood was drawn after 30, 60, 90, 120, 180, 240, 300 and 360 min for measurement of serum Ca, phosphorus (P), parathyroid hormone (PTH) and whole plasma calcitonin (iCT). All Ca supplements induced significant (+6.4% to +8.1%;p<0.01) increases in Ca and significant suppression of PTH (–37.4% to –57.4%;p<0.01). Comparison of response curves revealed significantly (p<0.01) more marked Ca increase and PTH suppression with CC than with the other three Ca salts. CG' and CC induced marginal decreases in serum P and the overall curve of P variations was different for TCP compared with CG, CG and CC. No significant variation of iCT was recorded during the test. We conclude that all four Ca supplements seem to be absorbed to some extent since they induce significant biochemical variations that may lead to a reduction in bone turnover and that CC induces a significantly larger increase in serum Ca and a significantly greater suppression of serum PTH. 相似文献
153.
I. Wessler D. J. Dooley J. Werhand F. Schlemmer 《Naunyn-Schmiedeberg's archives of pharmacology》1990,341(4):288-294
Summary Electrically-evoked release of [3H]acetylcholine from autonomic neurons (myenteric plexus), motoneurons (phrenic nerve) and the central nevous system (neocortex) was investigated in the presence and absence of the calcium channel antagonists -conotoxin GVIA, nifedipine and verapamil, whereby the same species (rat) was used in all experiments. Release of [3H]acetylcholine was measured after incubation of the tissue with [3H]choline.-Conotoxin GVIA markedly reduced (70%) the evoked release of [3H]acetylcholine from the myenteric plexus of the small intestine (IC50: 0.7 nmol/l) with a similar potency at 3 and 10 Hz stimulation. An increase in the extracellular calcium concentration attenuated the inhibitory effect of -conotoxin GVIA. Release of [3H]acetylcholine from the rat neocortex was also inhibited (90%) by -conotoxin GVIA, but the potency was 19-fold lower (IC50: 13 nmol/l). However, the release of [3H]acetylcholine from the phrenic nerve was not reduced by -conotoxin GVIA (100 nmol/l) at 1.8 mmol/l calcium (normal concentration), whereas -conotoxin GVIA inhibited evoked [3H]acetylcholine release by 47% at 0.9 mmol/l calcium. Neither nifedipine (0.1 and 1 mol/l) nor verapamil (0.1, 1 and 10 mol/l) modified the evoked release of [3H]acetylcholine from the myenteric plexus and the phrenic nerve.Acetylcholine release from different neurons appears to be regulated by different types of calcium channels. N-type channels play the dominant role in regulating acetylcholine release from both the myenteric plexus and the neocortex, whereas acetylcholine release from motor nerves is regulated by calcium channel(s) not yet characterized.
Send offprint requests to I. Wessler at the above address 相似文献
154.
Madhu S. Chintala Bhagavan S. Jandhyala 《Naunyn-Schmiedeberg's archives of pharmacology》1990,341(4):357-363
Summary The efficacy of felodipine, a dihydropyridine calcium entry blocker to restore renal function was investigated in Wiggers model of haemorrhagic shock. Mongrel dogs were anaesthetized with sodium pentobarbital and subjected to haemorrhagic shock by allowing the animals to bleed into a reservoir. After maintaining the hypotensive state (mean blood pressure 40–45 mm Hg) for a period of 150 min, the blood was reinfused and the recovery of the various parameters were monitored for an additional 120 min. These studies were conducted in three different groups of dogs: (A) Solvent control, (B) Felodipine 0.01 mol/kg i. v., administered 10 min prior to reinfusion of the blood, and (C) Felodipine 0.01 mol/kg i. v., administered prior to haemorrhage. In all the three groups arterial blood pressure returned to similar basal levels following reinfusion. Felodipine administration prior to haemorrhage or before reinfusion (Group B and C) resulted in a 80–95% recovery in the renal blood flow, 60–65% in the glomerular filtration rate, 15–300% in the urine volume and 80–100% in the urinary sodium and potassium excretions. In the vehicle-treated control group, despite a 45% recovery in the renal blood flow, renal function was not restored following reinfusion.The observations made in these studies suggest that felodipine, an arteriolar dilator which also possesses natriuretic properties, could be clinically useful in the treatment of renal failure in haemorrhagic shock. Prevention of cellular calcium overload during ischaemia and reperfusion by this dihydropyridine derivative, may account for its ability to preserve vascular as well as tubular function.
Send offprint requests to B. S. Jandhyala at the above address 相似文献
155.
An unidentified macromolecular inhibitory constituent of calcium oxalate crystal growth in human urine 总被引:3,自引:0,他引:3
Summary We have detected and isolated a macromolecular constituent in normal human urine possessing calcium crystal growth inhibitory activity. The purification procedure consisted of two anion exchange chromatographies and one affinity chromatography. The crystal growth inhibitor was found to be heterogeneous in net charge as well as in size. It has not been identified. It is not an uronic acid-containing glycosaminoglycan, hitherto presumed to be responsible for the inhibitory activity. Whether an urinary fragment of inter--trypsin inhibitor is responsible has yet to be resolved. 相似文献
156.
The effect of calcium-balanced heparin (471896, CIBA CORNING) on blood gas and electrolyte analysis was evaluated, by comparing with that of sodium heparin (Na heparin). One ml of whole blood was collected into a syringe, which contained calcium-balance heparin (Ca balanced heparin) or Na heparin. 122 pairs of blood samples obtained from 15 patients were analyzed for Na, K, ionized calcium (Ca(++)), total hemoglobin, pH, P(CO)(2), and P(O)(2) by an automatic blood gas and electrolyte analyzer, CIBA CORNING model 288. There was a significant difference ( P < 0.05) in pH, P(CO)(2), Na, and Ca(++) between the two different groups. Ca(++) concentration was significantly less in Na heparin group than in Ca balanced heparin group, probably due to more chelation of Ca(++) by Na heparin than Ca balanced heparin. The present study suggests that the Ca balanced heparin has minimal effect on the blood gas and electrolyte analysis, and is a suitable anticoagulant for the Ca(++) measurement. 相似文献
157.
Summary Experiments were carried out to elucidate the mechanism that the positive inotropic effect mediated by 1-adrenoceptors is more susceptible to organic calcium antagonists than the -adrenoceptor-mediated effect. Verapamil and diltiazem displaced the specific binding of [3H]prazosin to the membrane fraction derived from the rabbit ventricular myocardium, verapamil being about 70 times more potent than diltiazem. Nifedipine did not displace the binding. While these compounds suppressed the positive inotropic effect mediated via l-adrenoceptors in 1- concentration-dependent manner, there was no correlation between the potency of the compounds to displace the [3H]prazosin binding and to inhibit the -mediated positive inotropic effect. The relative potency of three calcium antagonists to decrease the basal force of contraction and the al-mediated effect (of the same extent as compared to basal force of contraction) was consistent to each other. The positive inotropic effect mediated by -adrenoceptors was inhibited much less, and was enhanced by low concentrations of organic calcium antagonists. The differential action of calcium antagonists on the - and -mediated positive inotropic effect was mimicked by lowering the extracellular calcium concentration to 1/2, 1/4 and 1/8 of that in normal Krebs-Henseleit solution (2.5 mmol/l). These results indicate that the 1-adrenoceptor blocking activity does not play an essential role for the preferential inhibition of -mediated positive inotropic effect by organic calcium antagonists. Difference in the subcellular mechanism involved in mobilization of intracellular Ca2+ subsequent to 1-and -adrenoceptor activation may be responsible for the differential inhibitory action of calcium antagonists in the rabbit heart.
Send offprint requests to M. Endoh at the above address 相似文献
158.
159.
血清锌、钙、锰含量对矮小儿童身高、骨龄的影响 总被引:1,自引:0,他引:1
目的:探讨血清锌、钙、锰含量对儿童身高、骨龄的影响。方法:用高频等离子体发射光谱法测定30例矮小儿童血清锌、钙、锰含量,同30例正常健康儿童比较。并进行锌、钙、锰与身高、骨龄相关分析。结果:矮小儿童血清锌、钙、锰含量明显低于对照组。相关分析发现,血清锌、钙、锰与身高呈明显正相关(P<0.01),血清锌、锰与骨龄呈明显正相关(P<0.01),而血清钙与骨龄无相关性(P>0.05)。结论:血清锌、钙、锰与儿童身高增长,骨龄成熟密切相关。 相似文献
160.
进一步研究氯丙烯的中毒机理,探讨氯丙烯对神经细胞内钙稳态与能量合成的影响。方法用Fura-2/AM、电子探针X线微区分析、ATP生物发光分析等方法测定氯丙烯染毒后鸡胚脑神经细胞内游离Ca2+、钙百分含量及ATP、ADP、AMP含量的改变。 结果随着氯丙烯浓度的增加,细胞内游离Ca2+浓度、钙百分含量明显增加(P 相似文献