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121.
Bo Hellman Janove Sehlin Inge-Bert Täljedal 《Pflügers Archiv : European journal of physiology》1978,378(2):93-97
Microdissected pancreatic islets of noninbredob/ob-mice were used to study ionic effects on the lanthanum-nondisplaceable45Ca2+ uptake by islet cells. Omission of Mg2+ from the incubation medium had no effect, but the45Ca2+ uptake was increased by omission of Na+ and decreased by omission of K+. Excess Mg2+ (1.2–15 mM) inhibited and excess K+ (4.7–25 mM) stimulated the45Ca2+ uptake in a concentration-dependent manner. Stimulation of45Ca2+ uptake in Na+-deficient islets was associated with an enhancement of the basal insulin release. Total abolishment of glucose-stimulated45Ca2+ uptake in K+-deficient islets did not preclude a significant secretory response to glucose. It is concluded that the lanthanum-nondisplaceable45Ca2+ uptake shows a partial correlation to insulin release. 相似文献
122.
Michael J. Taggart Theodor Burdyga Richard Heaton Susan Wray 《Pflügers Archiv : European journal of physiology》1996,432(5):803-811
Measurements of simultaneous force and intracellular Ca2+ concentration ([Ca2+]i) in rat uterine smooth muscle have been made to elucidate the mechanisms involved when force produced spontaneously, by high-K+ depolarization or carbachol is altered by a change of intracellular pH (pHi). Rises in force and [Ca2+]i were closely correlated for all forms of contraction, with the Ca2+ transient peaking before force. In spontaneously active preparations, alkalinization significantly increased, and acidification
decreased, force and [Ca2+]i. Inhibition of the sarcoplasmic reticulum ATPase (cyclopiazonic acid) did not affect these changes, whereas removal of external
Ca2+ abolished both responses, suggesting that the effect of pHi is on Ca2+ entry. Alkalinization caused a prolongation of the action potential complex, associated with a potentiation of contractile
activity. Acidification produced hyperpolarization and abolition of action potentials and spontaneous activity, but did not
prevent brief applications of carbachol or high-K+ from producing depolarization and increasing force, suggesting no impairment of the mechanism of generation of the action
potential. For depolarized preparations, acidification increased tonic force and [Ca2+]i; the increase in the calcium signal persisted in zero-external calcium. In the presence of carbachol, acidification transiently
increased force and [Ca2+]i, followed by a reduction in both. It is concluded that changes in pHi act at more than one step in excitation-contraction coupling and that changes in [Ca2+]i can account for most of the changes in uterine force.
Received: 1 April 1996 /Accepted: 8 May 1996 相似文献
123.
Previously we have reported that serotonin’s (5-hydroxytryptamine or 5-HT) potentiating action on L-type Ca channels is present
only in definite neurones from pedal ganglia of the mollusc Helix pomatia [Kostyuk PG, Lu kyanetz EA, Doroshenko PA (1992) Effects of serotonin and cAMP on calcium currents in different nevrones
of Helix pomatia. Pflügers Arch 420:9–15]. The potentiation is mediated by the cAMP second messenger system and is triggered by 5-HT1-like type receptors. To understand the physiological and pharmacological significance of this phenomenon, we analysed the
comparative effects of dopamine (DA) and 5-HT on voltage-operated Ca currents (I
ca) in isolated, intracellularly perfused H. pomatia neurones in whole- cell patch-clamp experiments. Two types of effects of DA (1–10 μM) and 5-HT (1–10 μM) on I
ca were observed in different neurones: reversible inhibition (by about 40% and 20% respectively) or reversible potentiation
(up to 65% and 40% respectively) of current amplitude. Neurones insensitive to neurotransmitter application were also observed.
DA could induce potentiation of I
ca only in the same neurones that were similarly sensitive to 5-HT. However, a similar correlation between inhibitory action
of neurotransmitters on I
ca was not observed. The potentiating effects of 5-HT and DA on I
ca were not additive and were mimicked by intracellular cAMP (100 μM) or 20 μg/ml of the catalytic subunit of protein kinase
A. We established that the potentiating effects of neurotransmitters were mediated by two distinct receptors, as the DA receptor
antagonist ergometrin (1 μM) selectively inhibited the enhancement of I
ca by DA and did not affect the action of 5-HT in the same cell. A similar specificity was observed for the dopaminergic compound,
5-chlortryptamine (10 μM), whereas the classical neuroleptic fluphenazine (10 μM) effectively blocked the 5-HT-evoked effect
without significantly changing the action of DA. Methiothepin, an antagonist of 5-HT1 and 5-HT2 receptors, blocked both 5-HT-and DA-evoked effects. The results point out a possible convergence of the two different receptors
(5-HT1-like and D1) on the same cAMP-dependent system of phosphorylation in the up-regulation of L-type Ca channel activity in mollusc neurones.
Received: 14 September 1995/Received after revision and accepted: 8 January 1995 相似文献
124.
H. M. Piper 《Journal of molecular medicine (Berlin, Germany)》1989,67(9):465-476
Summary After prolonged ischemia or hypoxia myocardial injury is not reversed but exacerbated by a resupply of the tissue with oxygen and substrates. The mechanism by which reversible ischemic or hypoxic myocardial injury becomes irreversible is not yet understood. It has been debated whether reperfusion injury merely uncovers pre-existing irreversible injury, or is indeed caused by the reperfusion/reoxygenation process. In recent years, three theories have been discussed that relate the onset of irreversibility either to: a critical energy loss; a critical accumulation of cellular calcium; or to the deleterious effects of free radical formation. In certain experimental models for each of these theories favourable results have been obtained. Current research suggests that absolute reversibility thresholds in energy depletion or calcium accumulation in the ischemic or hypoxic cell do not exist. A key role of free radical injury for reperfusion injury must also be questioned. There is, however, evidence that in tissue reversibility of ischemic cardiomyocyte injury is limited by conditions that make calcium-induced hypercontracture upon reoxygenation unavoidable. This occurs when, by hypercontracture, mutual mechanical disruption of the cells destroys the tissue. From isolated cardiomyocytes that are able to metabolically survive hypercontracture it has been observed that these metabolic conditions do not represent the last biological possibility to reverse injury. 相似文献
125.
M. Ritter E. Wöll S. Waldegger D. Häussinger H. J. Lang W. Scholz B. Schölkens F. Lang 《Pflügers Archiv : European journal of physiology》1993,423(3-4):221-224
In NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ras) bradykinin leads to sustained oscillations of cell membrane potential due to oscillations of intracellular Ca2+ with subsequent activation of Ca2+-sensitive K+ channels. In cells not expressing the oncogene (-ras), bradykinin leads only to a single transient hyperpolarization of the cell membrane. The present study has been performed to elucidate the possible interaction of cell volume, intracellular pH and bradykinin-induced oscillations of the cell membrane potential. Bradykinin leads to cell shrinkage and intracellular alkalinization of both +ras cells and –ras cells. Inhibition of Na+/H+ exchanger by HOE 694 abolishes the bradykinin-induced alkalinization but does not significantly interfere with the bradykinin-induced oscillations of cell membrane potential. In contrast, prevention of bradykinin-induced cell shrinkage by simultaneous reduction of extracellular osmolarity blunts the oscillations. Thus, cell shrinkage stimulates bradykinin-induced oscillations of cell membrane potential. On the other hand, cell shrinkage alone does not elicit oscillations unless, in addition, Ca2+ entry is stimulated by ionomycin. 相似文献
126.
B. Poch F. Gansauge S. Gansauge T. Anger U. Nilsson M. H. Schoenberg H. G. Beger 《Inflammation research》1996,45(8):428-433
Oxygen derived free radicals are involved in many pathological processes such as postischemic reperfusion injuries, hepatotoxicity of drugs and inflammatory processes. Thereby these oxygen radicals induce lipid peroxidation and perturbation of cellular membranes. The aim of our present study was to determine whether oxygen radicals generated by the xanthine oxidase/hypoxanthine system cause a release of histamine in human blood cell cultures. Stimulation of blood cell cultures with oxygen radicals induced a histamine liberation which was mainly due to calcium independent processes during the first 30 min, whereas then calcium requiring processes took part in the release of histamine. The regulation of the leukocyte selectin LECAM-1 was altered by oxygen radicals whereas histamine, which is known to modulate vascular selectin expression, did not affect the expression of LECAM-1. Our data indicate that oxygen radicals induce a direct calcium independent release of histamine which is due to membrane pertubating processes during the first phase but also induce a specific reaction leading to a further indirect histamine liberation which is probably mediated by PAF.accepted by W. LorenzThe first two authors contributed equally to this paper. 相似文献
127.
目的:研究SeO2对急性早幼粒细胞白血病细胞株NB4、红白血病细胞K562、急性粒细胞白血病细胞株HL-60的增生、凋亡、活性氧(ROS)及Ca2+水平等的影响。 方法: 采用不同浓度SeO2(3-30 μmol/L)分别处理3种白血病细胞,用流式细胞术测定细胞凋亡率、细胞中ROS和Ca2+的水平。 结果: 10和30 μmol/L SeO2能抑制3种细胞增生,30 μmol/L SeO2作用48 h能使54.0%的NB4细胞、46.5%的K562细胞和49.6%的HL-60细胞发生凋亡。同时下调细胞内ROS和Ca2+水平。NB4和HL-60细胞中ROS阳性细胞比例随SeO2浓度增加而减少,K562中只有30 μmol/L SeO2才能使ROS出现明显下降。10、30 μmol/L SeO2能使NB4和HL-60细胞内Ca2+水平逐步下降。K562中只有30 μmol/L SeO2才能使细胞内Ca2+水平出现明显下降。 结论: SeO2对3种白血病细胞均有诱导凋亡作用,在凋亡过程中涉及细胞内ROS及Ca2+水平下降。 相似文献
128.
目的:在培养的新生大鼠心肌细胞上,观察多种刺激因素对细胞胞浆Ca2+([Ca2+]c)和核Ca2+([Ca2+]n)的影响,探讨其时间和空间关系及其机制。方法:以Fluo-4/AM荧光指示剂负载培养的心肌细胞,应用激光共聚焦扫描显微镜检测胞浆和核Ca2+震荡的变化。结果:正常心肌细胞内核Ca2+的荧光强度高于核周与细胞浆,三者均存在小幅度的钙震荡,分别加入去甲肾上腺素(10-5mol/L)、异丙肾上腺素(10-4mol/L)和三磷酸腺苷(ATP3×10-3mol/L),均使心肌细胞钙震荡幅度明显升高(P<0.01),L-型Ca2+通道阻滞剂维拉帕米(verapamil5×10-4mol/L)、Ca2+-ATPase抑制剂thapsigargin(10-6mol/L)和KCl(20mmol/L)使钙的周期性震荡消失。用thapsigargin10-6mol/L预先阻断心肌细胞钙库的Ca2+摄取,去甲肾上腺素(10-5mol/L)则不能引起钙震荡和荧光强度增加。结论:心肌细胞胞浆和核Ca2+均能产生钙震荡,而钙震荡的维持则依赖于细胞外Ca2+的内流、胞内钙库的Ca2+摄取和释放以及正常膜电位的维持。核与胞浆Ca2+变化不一致,提示细胞核上可能存在相对独立的Ca2+调节系统。 相似文献
129.
D. von Herrath K. Schaefer J. P. Bonjour H. Fleisch 《Pflügers Archiv : European journal of physiology》1972,336(3):249-262
Summary The metabolism and the organ distribution of double labelled vitamin D3 (1,2-3H-4-14C-cholecalciferol) has been studied in rats in which the bone mineralization and the intestinal calcium absorption have been inhibited by a large pose (10 mg P/kg s.c. for 7–14 days) of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP). The most striking difference found was a reduced accumulation of radioactive cholecalciferol and its metabolites in the kidney of EHDP-treated rats. It is unlikely that this effect was due to an unspecific alteration of the functional renal tissue since blood urea, glomerular filtration rate and renal plasm a flow remained unaltered by this dose of EHDP. The EHDP-treated rats were able to form the metabolite eluted with peak IV of the silicic acid chromatographic system, that is 25-hydroxycholecalciferol. In these vitamin D repleted rats fed a high calcium diet, the tritium deficient metabolite eluted with peak V (1,25-dihydroxycholecalciferol) was only found in the intestinal mucosa of both control and EHDP groups three days after the injection of radioactive cholecalciferol, and this in a very small amount. Therefore no definitive conclusion can be drawn as to a possible interference of EHDP treatment on the production of 1,25-dihydroxycholecalciferol. The change in the renal metabolism of vitamin D in rats treated with a rachitogenic dose of EHDP may be caused by the modifications of the calcium metabolism brought about by the diphosphonate. Its relation, if any, with the decreased calcium absorption remains to be established. 相似文献
130.
Luis Gandía Baldomero Lara Julita S. Imperial Mercedes Villarroya Almudena Albillos Rosario Maroto A. G. García Baldomero M. Olivera 《Pflügers Archiv : European journal of physiology》1997,435(1):55-64
The characteristics of the binding sites for the Conus magus toxins ω-conotoxin MVIIC and ω-conotoxin MVIID, as well as their effects on K+-evoked 45Ca2+ entry and whole-cell Ba2+ currents (I
Ba), and K+-evoked catecholamine secretion have been studied in bovine adrenal chromaffin cells. Binding of [125I] ω-conotoxin GVIA to bovine adrenal medullary membranes was displaced by ω-conotoxins GVIA, MVIIC and MVIID with IC50 values of around 0.1, 4 and 100 nM, respectively. The reverse was true for the binding of [125I] ω-conotoxin MVIIC, which was displaced by ω-conotoxins MVIIC, MVIID and GVIA with IC50 values of around 30, 80 and 1.200 nM, respectively. The sites recognized by ω-conotoxins MVIIC and MVIID in bovine brain
exhibited higher affinities (IC50 values of around 1 nM). Both ω-conotoxin MVIIC and MVIID blocked I
Ba by 70–80%; the higher the [Ba2+]o of the extracellular solution the lower the blockade induced by ω-conotoxin MVIIC. This was not the case for ω-conotoxin
MVIID; high Ba2+ (10 mM) slowed down the development of blockade but the maximum blockade achieved was similar to that obtained in 2 mM Ba2+. A further difference between the two toxins concerns their reversibility; washout of ω-conotoxin MVIIC did not reverse the
blockade of I
Ba while in the case of ω-conotoxin MVIID a partial, quick recovery of current was produced. This component was irreversibly
blocked by ω-conotoxin GVIA, suggesting that it is associated with N-type Ca2+ channels. Blockade of K+-evoked 45Ca2+ entry produced results which paralleled those obtained by measuring I
Ba. Thus, 1 μM of each of ω-conotoxin GVIA and MVIIA inhibited Ca2+ uptake by 25%, while 1 μM of each of ω-conotoxin MVIIC and MVIID caused a 70% blockade. K+-evoked catecholamine secretory responses were not reduced by ω-conotoxin GVIA (1 μM). In contrast, at 1 μM both ω-conotoxin
MVIIC and MVIID reduced the exocytotic response by 70%. These data strengthen the previously established conclusion that Q-type
Ca2+ channels that contribute to the regulation of secretion and are sensitive to ω-conotoxins MVIIC and MVIID are present in
bovine chromaffin cells. These channels, however, seem to possess binding sites for ω-conotoxins MVIIC and MVIID whose characteristics
differ considerably from those described to occur in the brain; they might represent a subset of Q-type Ca2+ channels or an entirely new subtype of voltage-dependent high-threshold Ca2+ channel.
Received: 16 April 1997 / Received after revision: 10 July 1997 / Accepted: 23 July 1997 相似文献