Academic literature on the topic 'Intracellular Calcium Transient'
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Journal articles on the topic "Intracellular Calcium Transient"
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Xie, Lai-Hua, and James N. Weiss. "Arrhythmogenic consequences of intracellular calcium waves." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 3 (2009): H997—H1002. http://dx.doi.org/10.1152/ajpheart.00390.2009.
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Intracellular Ca2+ (Cai2+) waves are known to cause delayed afterdepolarizations (DADs), which have been associated with arrhythmias in cardiac disease states such as heart failure, catecholaminergic polymorphic ventricular tachycardia, and digitalis toxicity. Here we show that, in addition to DADs, Cai2+ waves also have other consequences relevant to arrhythmogenesis, including subcellular spatially discordant alternans (SDA, in which the amplitude of the local Cai2+ transient alternates out of phase in different regions of the same cell), sudden repolarization changes promoting the dispersion of refractoriness, and early afterdepolarizations (EADs). Cai2+ was imaged using a charge-coupled device-based system in fluo-4 AM-loaded isolated rabbit ventricular myocytes paced at constant or incrementally increasing rates, using either field stimulation, current clamp, or action potential (AP) clamp. Cai2+ waves were induced by Bay K 8644 (50 nM) + isoproterenol (100 nM), or low temperature. When pacing was initiated during a spontaneous Cai2+ wave, SDA occurred abruptly and persisted during pacing. Similarly, during rapid pacing, SDA typically arose suddenly from spatially concordant alternans, due to an abrupt phase reversal of the subcellular Cai2+ transient in a region of the myocyte. Cai2+ waves could be visualized interspersed with AP-triggered Cai2+ transients, producing a rich variety of subcellular Cai2+ transient patterns. With free-running APs, complex Cai2+ release patterns were associated with DADs, EADs, and sudden changes in AP duration. These findings link Cai2+ waves directly to a variety of arrhythmogenic phenomena relevant to the intact heart.
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Fuchs, Andreas, Marcel Rigaud, Constantine D. Sarantopoulos, Patrick Filip, and Quinn H. Hogan. "Contribution of Calcium Channel Subtypes to the Intracellular Calcium Signal in Sensory Neurons." Anesthesiology 107, no. 1 (2007): 117–27. http://dx.doi.org/10.1097/01.anes.0000267511.21864.93.
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Abstract Background: Although the activation-induced intracellular Ca2+ signal is disrupted by sensory neuron injury, the contribution of specific Ca2+ channel subtypes is unknown. Methods: Transients in dissociated rat dorsal root ganglion neurons were recorded using fura-2 microfluorometry. Neurons from control rats and from neuropathic animals after spinal nerve ligation were activated either by elevated bath K+ or by field stimulation. Transients were compared before and after application of selective blockers of voltage-activated Ca2+ channel subtypes. Results: Transient amplitude and area were decreased by blockade of the L-type channel, particularly during sustained K+ stimulation. Significant contributions to the Ca2+ transient are attributable to the N-, P/Q-, and R-type channels, especially in small neurons. Results for T-type blockade varied widely between cells. After injury, transients lost sensitivity to N-type and R-type blockers in axotomized small neurons, whereas adjacent small neurons showed decreased responses to blockers of R-type channels. Axotomized large neurons were less sensitive to blockade of N- and P/Q-type channels. After injury, neurons adjacent to axotomy show decreased sensitivity of K+-induced transients to L-type blockade but increased sensitivity during field stimulation. Conclusions: All high-voltage–activated Ca2+ current subtypes contribute to Ca2+ transients in sensory neurons, although the L-type channel contributes predominantly during prolonged activation. Injury shifts the relative contribution of various Ca2+ channel subtypes to the intracellular Ca2+ transient induced by neuronal activation. Because this effect is cell-size specific, selective therapies might potentially be devised to differentially alter excitability of nociceptive and low-threshold sensory neurons.
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Katra, Rodolphe P., Etienne Pruvot, and Kenneth R. Laurita. "Intracellular calcium handling heterogeneities in intact guinea pig hearts." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 2 (2004): H648—H656. http://dx.doi.org/10.1152/ajpheart.00374.2003.
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Regional heterogeneities of ventricular repolarizing currents and their role in arrhythmogenesis have received much attention; however, relatively little is known regarding heterogeneities of intracellular calcium handling. Because repolarization properties and contractile function are heterogeneous from base to apex of the intact heart, we hypothesize that calcium handling is also heterogeneous from base to apex. To test this hypothesis, we developed a novel ratiometric optical mapping system capable of measuring calcium fluorescence of indo-1 at two separate wavelengths from 256 sites simultaneously. With the use of intact Langendorff-perfused guinea pig hearts, ratiometric calcium transients were recorded under normal conditions and during administration of known inotropic agents. Ratiometric calcium transients were insensitive to changes in excitation light intensity and fluorescence over time. Under control conditions, calcium transient amplitude near the apex was significantly larger (60%, P < 0.01) compared with the base. In contrast, calcium transient duration was significantly longer (7.5%, P < 0.03) near the base compared with the apex. During isoproterenol (0.05 μM) and verapamil (2.5 μM) administration, ratiometric calcium transients accurately reflected changes in contractile function, and, the direction of base-to-apex heterogeneities remained unchanged compared with control. Ratiometric optical mapping techniques can be used to accurately quantify heterogeneities of calcium handling in the intact heart. Significant heterogeneities of calcium release and sequestration exist from base to apex of the intact heart. These heterogeneities are consistent with base-to-apex heterogeneities of contraction observed in the intact heart and may play a role in arrhythmogenesis under abnormal conditions.
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Whitaker, M., and R. Patel. "Calcium and cell cycle control." Development 108, no. 4 (1990): 525–42. http://dx.doi.org/10.1242/dev.108.4.525.
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The cell division cycle of the early sea urchin embryo is basic. Nonetheless, it has control points in common with the yeast and mammalian cell cycles, at START, mitosis ENTRY and mitosis EXIT. Progression through each control point in sea urchins is triggered by transient increases in intracellular free calcium. The Cai transients control cell cycle progression by translational and post-translational regulation of the cell cycle control proteins pp34 and cyclin. The START Cai transient leads to phosphorylation of pp34 and cyclin synthesis. The mitosis ENTRY Cai transient triggers cyclin phosphorylation. The motosis EXIT transient causes destruction of phosphorylated cyclin. We compare cell cycle regulation by calcium in sea urchin embryos to cell cycle regulation in other eggs and oocytes and in mammalian cells.
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Kotlikoff, M. I., R. K. Murray, and E. E. Reynolds. "Histamine-induced calcium release and phorbol antagonism in cultured airway smooth muscle cells." American Journal of Physiology-Cell Physiology 253, no. 4 (1987): C561—C566. http://dx.doi.org/10.1152/ajpcell.1987.253.4.c561.
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Primary cultures of airway smooth muscle cells were exposed to histamine, and intracellular free calcium transients were measured by the calcium-sensitive dye fura-2. Stimulation with 100 microM histamine resulted in a rise in intracellular calcium from an unstimulated level of 178 +/- 25 to 497 +/- 154 nM Ca2+ (SE; n = 14) and a return to base-line free calcium concentration within 1 min of stimulation. Pretreatment of cells with the H1 receptor blocker pyrilamine (2.5 microM) abolished the response; however, the calcium transient was not altered by pretreatment with the H2 blocker cimetidine (50 microM), by chelation of external calcium, or by pretreatment with 2 mM Co2+ or 5 microM nifedipine. Activation of protein kinase c by 200 nM phorbol 12-myristate 13-acetate (PMA) resulted in no detectable rise in cytosolic calcium but completely blocked the release of internal calcium by histamine. We conclude that 1) histamine causes a transient rise of cytosolic calcium in airway smooth muscle, 2) the rise in cytosolic calcium is mediated by H1 receptor coupling that triggers release of internal calcium stores, and 3) activation of protein kinase c blocks the histamine-induced release of intracellular calcium.
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Appleby, Peter A., Saqib Shabir, Jennifer Southgate, and Dawn Walker. "Cell-type-specific modelling of intracellular calcium signalling: a urothelial cell model." Journal of The Royal Society Interface 10, no. 86 (2013): 20130487. http://dx.doi.org/10.1098/rsif.2013.0487.
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Calcium signalling plays a central role in regulating a wide variety of cell processes. A number of calcium signalling models exist in the literature that are capable of reproducing a variety of experimentally observed calcium transients. These models have been used to examine in more detail the mechanisms underlying calcium transients, but very rarely has a model been directly linked to a particular cell type and experimentally verified. It is important to show that this can be achieved within the general theoretical framework adopted by these models. Here, we develop a framework designed specifically for modelling cytosolic calcium transients in urothelial cells. Where possible, we draw upon existing calcium signalling models, integrating descriptions of components known to be important in this cell type from a number of studies in the literature. We then add descriptions of several additional pathways that play a specific role in urothelial cell signalling, including an explicit ionic influx term and an active pumping mechanism that drives the cytosolic calcium concentration to a target equilibrium. The resulting one-pool model of endoplasmic reticulum (ER)-dependent calcium signalling relates the cytosolic, extracellular and ER calcium concentrations and can generate a wide range of calcium transients, including spikes, bursts, oscillations and sustained elevations in the cytosolic calcium concentration. Using single-variate robustness and multivariate sensitivity analyses, we quantify how varying each of the parameters of the model leads to changes in key features of the calcium transient, such as initial peak amplitude and the frequency of bursting or spiking, and in the transitions between bursting- and plateau-dominated modes. We also show that, novel to our urothelial cell model, the ionic and purinergic P2Y pathways make distinct contributions to the calcium transient. We then validate the model using human bladder epithelial cells grown in monolayer cell culture and show that the model robustly captures the key features of the experimental data in a way that is not possible using more generic calcium models from the literature.
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Nüße, Oliver, та Manfred Lindau. "GTPγS-induced calcium transients and exocytosis in human neutrophils". Bioscience Reports 10, № 1 (1990): 93–103. http://dx.doi.org/10.1007/bf01116857.
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Exocytosis and intracellular free calcium ([Ca2+]in) were simultaneously recorded in single human neutrophils using patch-clamp capacitance measurements and the fura-2 fluorescence ratio method. Intracellular application of guanosine-5′-O(3-thiotriphosphate) (GTPγS) stimulates both exocytosis and a calcium transient. The calcium transient starts to develop after a lag phase of ∼40s and normally appears to trigger the onset of exocytosis indicated by the beginning of the capacitance increase. After this delay [Ca2+]in increases from ∼150 nM to ∼600 nM with a sigmoidal time course. The peak concentration is reached within ∼30 s but the main increase occurs during ∼ 3s. [Ca2+]in subsequently decays within 1–2 min to a level which is close to the resting value. This calcium transient is due to calcium release from inositoltrisphosphate-sensitive intracellular stores. Exocytosis also occurs if the calcium transient is abolished by intracellular EGTA but the lag phase is markedly prolonged. The GTPγS-induced calcium transient is very similar to that observed after stimulation with N-formyl-methionyl-leucyl-phenylalanine. The interplay between guanine nucleotides, [Ca2+]in and exocytosis in neutrophils closely resembles previous results obtained in mast cells suggesting a similar regulation of exocytosis in both cell types.
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Fisher, T. E., S. Levy, and L. K. Kaczmarek. "Transient changes in intracellular calcium associated with a prolonged increase in excitability in neurons of Aplysia californica." Journal of Neurophysiology 71, no. 3 (1994): 1254–57. http://dx.doi.org/10.1152/jn.1994.71.3.1254.
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1. Transient stimulation of an afferent input to the bag cell neurons of Aplysia californica triggers a 30-min period of spontaneous firing termed the afterdischarge. Measurement of free calcium ion concentrations using calcium-sensitive electrodes revealed a biphasic pattern of elevation of intracellular calcium levels during the afterdischarge. Basal calcium levels at the soma were found to rise rapidly during afferent stimulation and then to decline before the onset of spontaneous firing. This early peak in intracellular calcium was followed by a slower, transient elevation of calcium levels during the period of rapid firing that occurs in the first few minutes of afterdischarge. Stimulation of clusters of bag cell neurons in a calcium-free external medium failed to trigger afterdischarge and produced no changes in basal intracellular calcium levels. 2. When calcium ions in the external medium were replaced by barium ions, stimulation of clusters of bag cell neurons triggered afterdischarges that were characterized by long-duration action potentials. Intracellular calcium levels during these afterdischarges rose slowly over the first few minutes of spontaneous firing. Because calcium-sensitive microelectrodes do not respond to barium ions, these data suggest that stimulation of afterdischarge triggers calcium release from an intracellular compartment. 3. During afterdischarges in barium-containing external media, each broadened action potential produced a discrete transient elevation of intracellular calcium levels. A similar effect was observed in isolated bag cell neurons in primary culture when action potentials were stimulated by depolarizing current pulses in a barium-containing medium. These data suggest that, under these conditions, individual action potentials trigger the release of intracellular calcium from some intracellular pool.
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Ittichaicharoen, Jitjiroj, Nattayaporn Apaijai, Pongpan Tanajak, Piangkwan Sa-nguanmoo, Nipon Chattipakorn, and Siriporn C. Chattipakorn. "Impaired mitochondria and intracellular calcium transients in the salivary glands of obese rats." Applied Physiology, Nutrition, and Metabolism 42, no. 4 (2017): 420–29. http://dx.doi.org/10.1139/apnm-2016-0545.
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Long-term consumption of a high-fat diet (HFD) causes not only obese-insulin resistance, but is also associated with mitochondrial dysfunction in several organs. However, the effect of obese-insulin resistance on salivary glands has not been investigated. We hypothesized that obese-insulin resistance induced by HFD impaired salivary gland function by reducing salivation, increasing inflammation, and fibrosis, as well as impairing mitochondrial function and calcium transient signaling. Male Wistar rats (200–220 g) were fed either a ND or an HFD (n = 8/group) for 16 weeks. At the end of week 16, salivary flow rates, metabolic parameters, and plasma oxidative stress were determined. Rats were then sacrificed and submandibular glands were removed to determine inflammation, fibrosis, apoptosis, mitochondrial function and dynamics, and intracellular calcium transient signaling. Long-term consumption of an HFD caused obese-insulin resistance and increased oxidative stress, fibrosis, inflammation, and apoptosis in the salivary glands. In addition, impaired mitochondrial function, as indicated by increased mitochondrial reactive oxygen species, mitochondrial membrane depolarization, and mitochondrial swelling in salivary glands and impaired intracellular calcium regulation, as indicated by a reduced intracellular calcium transient rising rate, decay rates, and amplitude of salivary acinar cells, were observed in HFD-fed rats. However, salivary flow rate and level of aquaporin 5 protein were not different between both groups. Although HFD consumption did not affect salivation, it caused obese-insulin resistance, leading to pathophysiological alteration of salivary glands, including impaired intracellular calcium transients, increased oxidative stress and inflammation, and salivary mitochondrial dysfunction.
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Bird, Stephen D., and Robert J. Walker. "Mast Cell Histamine-Induced Calcium Transients in Cultured Human Peritoneal Mesothelial Cells." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 18, no. 6 (1998): 626–36. http://dx.doi.org/10.1177/089686089801800611.
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Objective Peritoneal inflammation results from a complex interplay of events initiated by macrophage activity in response to infection, with the stimulation of mesothelial cell cytokine release amplifying the recruitment of blood-borne defense cells to the site of injury. Resident peritoneal mast cells may add to this complexity with mast cell derived cytokines released during this cascade. This study examined the influence of histamine, a mast cell derived inflammatory mediator, on the initial activation of human peritoneal mesothelial cells (HPMC) by intracellular free calcium (Cai2+) mobilization, and changes to the actin cytoskeleton. Design HPMC signal transduction was examined in response to histamine (1.0 mmol/L) compared to fetal bovine serum (FBS) (0.1 %) and 4-br-A23187 (1.0 μmol/L). Intracellular free calcium was measured in fura-2 loaded cells with and without external calcium (Ca2ex+t), or Ca2ex+t with verapamil (100 μmol/L). Following treatment with agonists, HPMC actin cytoskeleton was stained using direct immunocytochemistry. Results HPMC responded to histamine with a twofold transient rise in Cai2+ which returned to the baseline, in contrast with FBS and A23187–induced Cai2+ transients, which returned to elevated resting values. In the absence of Ca2ex+t’ all agents produced a calcium transient indicative of calcium release from intracellular stores. Histamine induced calcium -dependent changes to the cytoskeleton and cellular organization, including increased actin stress fibers. Conclusion Histamine produced large specific receptor-mediated calcium transients in HPMC, which included components of calcium release from intracellular stores and receptor -mediated calcium influx processes. The observed response to histamine raises the possibility that histamine derived from resident mast cells may modulate mesothelial cell function, in part by calciumdependent pathways, and influence the performance of the peritoneal membrane during peritoneal dialysis.
Dissertations / Theses on the topic "Intracellular Calcium Transient"
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Negretti, Sanchez Nilda Rosa. "Control of the systolic calcium transient by sacrolemmal and intracellular mechanisms in rat ventricular myocytes." Thesis, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385274.
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Wang, Ken. "Utility and limitations of cardiac tissue slices for the study of cardiac electrophysiology." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:a1ec53bd-263f-4814-8fcd-dc47a08bc00e.
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Cardiac tissue slices, a rarely used pseudo two-dimensional preparation, have gained increasing popularity for applications such as drug testing over the last ten years as they combine ease of handling with patho-physiologically relevant cell-type representation, distribution and inter-connection. The most well-established methods to measure electrophysiology in cardiac tissue are sharp electrodes and multi-electrode-arrays, techniques which are limited in spatial resolution or signal content. In this work, we have applied dual voltage Ca<sup>2+</sup> optical mapping on cardiac slices, allowing us to record these two key parameters simultaneously at high spatio-temporal resolution, yielding better visualisation of conduction waves, spatial dispersion in action potential (AP) characteristics, and intracellular Ca<sup>2+</sup> transient (CaT). The slice preparation method and the measurement protocols were refined to yield good reproducibility. Data analysis routines were developed to extract relevant parameters reliably. Despite being a promising candidate for drug testing, little is known about how slice and intact whole-heart AP properties are interrelated, and how to scale-up from observations in two dimensions (2D) to the three dimensional (3D) heart. In this thesis, we present a method to compare directly AP properties of intact whole-heart and tissue slices, and show the extent to which slices preserve AP characteristics. We have explored the suitability of tissue slices as an experimental model to study stretch induced changes in AP and CaT. During axial stretch, a dynamic profile of both AP and CaT was observed with an initial shortening of both AP and CaT duration, followed by a gradual recovery/prolongation. We have also used tissue slices to study spatial heterogeneity of AP and CaT properties in the rabbit left ventricular free wall. A transmural gradient can be captured in CaT and AP (with the longest APD and CaT durations being captured in the subendocardium). No large AP prolongation was found in the mid-myocardium. We conclude that the cardiac tissue slice preparation preserves some key functional parameters of the whole heart and is a promising model to study cardiac electrophysiology.
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Britto, Raquel Moreira de. "Efeito da fração aquosa das folhas de Costus spiralis (Jacq.) Roscoe sobre a função contrátil do coração de mamíferos." Universidade Federal de Sergipe, 2011. https://ri.ufs.br/handle/riufs/3748.
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Teas and infusions from C. spiralis leaf have largely been used by folk medicine as diuretic, hypotensor, cytotoxic, immunomodulator, antilithiasic, antidiarrheic, antispasmodic, antiurolitic, antimicrobian, antifungic, antioxidant, antileishmania activity, antiinflamatory, and antiedematogenic activity. In spite of these biological effects attributed to the extracts of C. spiralis, nothing so far could be found in the scientific literature dealing with its effects on the mammalian myocardium.The present study aimed to describe the inotropic effects
produced by extracts from the C. spiralis leaf on isolated guinea pig atrium, as well as to contribute for a better understanding about its mechanism of action in that
tissue. In isolated mouse cardiomyocytes, the effect produced by those extracts on the intracellular calcium transient and on the sarcolemal L-type calcium current were also measured. Experiments performed to evaluate the contractile effects were carried out on isolated atrium from guinea pig (Cavia porcellus). Firstly, our
purpose was to determine the most potent fraction obtained from the C. spiralis leaf. This was done by comparing the hydroalchoolic crude extract with the following ones: aqueous, chloroform, and ethyl acetate. A phytochemical analysis was performed on the fraction exhibiting the greater potency. This evaluation followed
the procedures proposed by Matos (1997). The content of sodium and potassium in the most potent fraction was determined by flame photometry. In the contractile
experiments, the atrial force was measured isometrically. Biological signals were captured, amplified, and then stored in computer to be processed off line. Intracellular calcium transients were studied by confocal microscopy with laser scanning by using the fluorescent dye FLUO 4AM. Calcium inward currents were
measured in mouse cardiomyocytes by using patch clamp technique in the whole cell configuration. Yield percentage of the aqueous fraction (AqF) was 69,40%.
This fraction showed the most potent depressor effect on the myocardial contractility (EC50 = 305 ± 41,00 mg/L, Hill constant = 1,46 ± 0,19). The following metabolites were found in the AqF: tannins, saponins, and polifenols (flavonol, flavononol, flavone, xanthone, phenol, and flavonoid). The potassium and sodium contents in 1 g/L of AqF were 1,91 and 0,15 mM, respectively. This was not enough to change the
myocardial inotropism, even in the highest concentration of AqF used in the experiments. The contraction and the relaxation time, as well as the time related to
the excitation-contraction coupling (stimulus-response) were not modified by adding AqF to the organ bath. However, AqF reduced the Efficiency Index for the
contraction and relaxation phases. The Neyler & Merrillees protocol was employed to evaluate the AqF effect on the calcium inward current in myocardial cells. Our results showed that AqF is able to completely abolish the Bowditch phenomenon, suggesting that it could be acting by reducing the sarcolemal calcium current. Supported by those experimental evidences, experiments were proposed to better understand the relationship between AqF and calcium mechanisms in cardiac cells. The following results were obtained with 1,5 g/L AqF: 1) AqF completely abolished the positive inotropic effect induced by isoproterenol (10-1 to 103 pM); 2) AqF shifted rightwardly the concentration-effect curve for CaCl2 (0.5 to 7.0 mM) and increased the EC50 from 1.12 ± 0.07 (Hill = 1.5) to 7.23 ± 0.47 mM (Hill = 7.4) (n = 3; p < 0.05); 3) AqF completely abolished the positive inotropic effect of (-) BAY K8644 (5 to 2000 nM); 4) AqF reduced the intracellular fluorescence from 4.66 ±1.17 to 3.74 ± 1.0 a.u. (n = 30 cells, 4 mice, p < 0.05); 5) AqF did not modify the decay rate of the fluorescent signal (892 ± 37 to 930 ± 30 ms, n = 30 cells, 4 mice, p > 0.05), indicating that it does not interfiere with the calcium removal from the sarcoplasm; 6) AqF reduced the calcium inward current through L-type calcium channels from 6,29 ± 0,34 to 4,9 ± 0,2 A/F (23% , n = 5 animals, p < 0,05). This study brought us unto the following conclusions: 1) AqF is the most potent fraction obtained from C. spirallis leaves; 2) AqF contains the following secondary metabolites: tannins, saponins, and poliphenols; 3) AqF reduces the contraction force of the guinea pig left atrium; 4) AqF acts on the myocardium contractility by reducing the calcium entry in myocardial cells during contraction.<br>Preparados de Costus spiralis têm sido usados pela medicina popular (diurético, hipotensor, citotóxico, imunomodulador, antilitiásico, antidiarréico, antiespasmódico, antiurolítico, antimicrobiano, antifúngico, antioxidante, antileishmânia, anti-inflamatório e antiedematogênico). Apesar da gama de ações a eles atribuídas, nada pôde ser encontrado na literatura científica com respeito ao possível efeito dos
Este trabalho visou determinar os efeitos inotrópicos obtidos das folhas de C. spiralis, que apresentava
maior potência, bem como contribuir para o mecanismo de ação desse preparado no miocárdio de mamíferos. Os experimentos sobre contração foram realizados em átrio esquerdo de cobaia (Cavia porcellus), enquanto que as medidas de transiente de cálcio intracelular e de corrente de membrana foram feitas em cardiomiócitos de camundongo. A investigação fitoquímica do preparado mais ativo foi conduzida segundo Matos (1997). Os teores de sódio e de potássio presentes na fração mais potente, foram determinados por fotometria de chama. A força de contração atrial foi captada isometricamente e, depois amplificada, foi armazenada em computador. O transiente de cálcio intracelular foi avaliado com microscopia confocal de varredura a laser. As correntes de cálcio sarcolemais foram medidas em cardiomiócitos submetidos à técnica do patch clamp ( whole cell ). A
fração aquosa (FAq) foi a que apresentou maior rendimento (69,40%) e a que exerceu maior efeito inotrópico negativo (CE50 = 305 ± 41,00 mg/L, Hill = 1,46 ± 0,19). Na sua constituição foram detectadas as seguintes classes de metabólitos secundários: taninos e saponinas, com reação fortemente positiva, e os polifenóis, com reação positiva (flavonóis, flavononóis, flavonas, xantonas, fenóis e flavonóides). Em 1 g/L de FAq foram encontrados 1,91 mM de potássio e 0,15 mM
de sódio. A adição de FAq ao Tyrode não modificou significativamente a concentração desses íons. Os tempos de contração e de relaxamento, bem como o
tempo de acoplamento eletromecânico não foram alterados pela FAq. Contudo, ela reduziu os Índices de Eficiência da contração e do relaxamento. A FAq aboliu
completamente o fenômeno de Bowditch induzido por alta frequência de estimulação, indicando que ela reduz a entrada desse íon nas células. Com base nessa
evidência, foram realizados protocolos para aprofundar o conhecimento sobre a participação das correntes de cálcio no mecanismo cardiodepressor da FAq. Esta
fração produziu os seguintes resultados: 1) aboliu completamente o efeito inotrópico positivo do isoproterenol (10-1 a 103 pM); 2) deslocou para a direita a curva concentração-efeito para o CaCl2 (0,5 a 7,0 mM), aumentando a CE50 de 1,12 ± 0,07 (Hill = 1,5) para 7,23 ± 0,47 mM (Hill = 7,4) (n = 3; p < 0,05); 3) aboliu
completamente o efeito inotrópico positivo do (-) BAY K8644 (5 a 2000 nM); 4) reduziu em cerca de 20% o pico da fluorescência intracelular correspondente ao
transiente de cálcio citoplasmático (controle: n = 30 células; teste: n = 27 células; 4 animais); 5) não modificou a velocidade de decaimento do sinal de fluorescência, o que significa que ela não interfere com o funcionamento da bomba de cálcio do retículo sarcoplasmático; 6) reduziu em 23% a densidade de corrente de cálcio tipo-L que variou de -6,29 ± 0,34 para -4,9 ± 0,2 A/F (n = 5 animais, p < 0,05). 1) a FAq foi a fração com maior potência inotrópica; 2) os principais metabólitos secundários presentes na FAq foram taninos, saponinas e polifenóis; 3) a FAq reduz
a força de contração do átrio; 4) o mecanismo da ação cardiodepressora da FAq sobre a contratilidade miocárdica se deve à diminuição da disponibilização do cálcio durante a contração.
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Gorbunova, Yuliya V. "Dynamics of intracellular messenger interactions : slow cAMP oscillations and spontaneous calcium transients /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3022180.
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Zhang, Jie. "The effects of cholesterol manipulation on contractions and intracellular calcium transients in human myometrium." Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.443930.
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Kassiri, Zamaneh. "Frequency- and hypertrophy-mediated alterations in twitch force and intracellular calcium transients in rat cardiac trabecula." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34088.pdf.
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Cori, Dario. "Descrizione e analisi quantitativa dei meccanismi di gestione del calcio intracellulare nei cardiomiociti derivati da staminali pluripotenti indotte." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2017. http://amslaurea.unibo.it/14749/.
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L'obiettivo di questa tesi è quello di migliorare l'attuale formulazione del primo modello finora sviluppato di cardiomiociti derivati da hiPSC, il Paci2013, attraverso l'utilizzo: i)di un set di dati sperimentali di transienti di Ca2+ e ii) di una procedura automatica per l’ottimizzazione dei parametri del modello. Il lavoro svolto per questa tesi si articola in diverse fasi. Dapprima è stata introdotta nel modello una nuova formulazione del rilascio di Ca2+ dal reticolo sarcoplasmatico, che riproduce in maniera più realistica un importante fenomeno alla base della contrazione muscolare cardiaca. Successivamente è stata effettuata una discriminazione dei dati sperimentali dei transienti di Ca2+ tramite una procedura di classificazione non supervisionata, al fine di rendere il set di misure sperimentali più consistente con il modello in esame. In seguito è stato implementato un framework di ottimizzazione parametrica che, tramite la minimizzazione di una funzione costo, ha consentito di calibrare il modello sulla base dei dati sperimentali. Infine, in fase di validazione del modello, sono state effettuate delle simulazioni di bloccanti di corrente per valutare che gli effetti di tali bloccanti sul potenziale d’azione fossero consistenti con dati sperimentali da letteratura. In conclusione, questo lavoro di tesi ha fornito in primis una nuova versione del modello Paci2013 calibrata su dati sperimentali di transienti di Ca2+ ed il framework di ottimizzazione parametrica, che rappresenta uno strumento utile per lo sviluppo di modelli computazionali.
Books on the topic "Intracellular Calcium Transient"
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Kassiri, Zamaneh. Frequency-and hypertrophy-mediated alterations in twith force and intracellular calcium transients in rat cardiac trabecula. National Library of Canada, 1998.
Find full textBook chapters on the topic "Intracellular Calcium Transient"
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Bosnjak, Zeljko J. "Effects of Volatile Anesthetics on the Intracellular Calcium Transient and Calcium Current in Cardiac Muscle Cells." In Advances in Experimental Medicine and Biology. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5979-1_9.
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Housmans, Philippe R. "The Relation Between Contraction Dynamics and the Intracellular Calcium Transient in Mammalian Cardiac Muscle." In Developments in Cardiovascular Medicine. Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1313-4_5.
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Gherardi, Gaia, and Cristina Mammucari. "Ex Vivo Measurements of Ca2+ Transients in Intracellular Compartments of Skeletal Muscle Fibers by Means of Genetically Encoded Probes." In Calcium Signalling. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9018-4_9.
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Loeb, Alex L., Nicholas J. Izzo, Randolph M. Johnson, James C. Garrison, and Michael J. Peach. "Intracellular Calcium Transients Associated with Endothelium-Derived Relaxing Factor Release May Be Mediated by Inositol-1,4,5-Trisphosphate." In Cell Calcium Metabolism. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_22.
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Endoh, Masao. "Frequency-Dependent Inhibition of the Intracellular Calcium Transients by Calmodulin Antagonists in the Aequorin-Injected Rabbit Papillary Muscle." In Calcium Protein Signaling. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5679-0_49.
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Saeki, Yasutake, Satoshi Kurihara, Kenichi Hongo, and Etsuko Tanaka. "Tension and Intracellular Calcium Transients of Activated Ferret Ventricular Muscle in Response to Step Length Changes." In Mechanism of Myofilament Sliding in Muscle Contraction. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2872-2_57.
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Endoh, Masao. "Regulation of force and intracellular calcium transients by cyclic AMP generated by forskolin, MDL 17,043 and isoprenaline, and its modulation by muscarinic receptor agents: a novel mechanism for accentuated antagonism." In Inotropic Stimulation and Myocardial Energetics. Steinkopff, 1989. http://dx.doi.org/10.1007/978-3-662-07908-9_8.
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Benarroch, Eduardo E. "Intracellular Signaling." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0003.
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Interactions between cells in the nervous system are bidirectional and involve a large number of chemical signals. These interactions occur via receptors located at presynaptic terminals, postsynaptic processes, or at a distance. Activation of membrane receptors by neurotransmitters, growth factors, cytokines, or other extracellular signals triggers downstream intracellular signaling pathways that affect a wide range of cellular functions. The final common mechanism is regulation of the state of phosphorylation of multiple crucial proteins in membranes, cytosol, cytoskeleton, and nucleus. The coupling between extracellular signals and these intracellular responses depends on transduction pathways that include G proteins that function as molecular switches; second messenger molecules such as cyclic nucleotides and phosphatidylinositol metabolites; intracellular calcium transients; and activation of protein kinases and phosphatases. Alterations of these fundamental cellular mechanisms provide the bases for a large number of disorders of the nervous system as well as potential therapeutic targets.
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Lowenstam, Heinz A., and Stephen Weiner. "Some Nonskeletal Functions in Biomineralization." In On Biomineralization. Oxford University Press, 1989. http://dx.doi.org/10.1093/oso/9780195049770.003.0012.
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The functions of mineralized hard parts are often self-evident. In many of the tables throughout the book we note the assigned or very often assumed functions of many different mineralized bodies. Often, however, assumed functions do not stand up to closer examination. A good example is the study of the cells of the hepatopancreas of gastropods (Howard et al. 1981). These glands have numerous cells containing intracellular mineralized granules. It was generally assumed that they all functioned as transient storage sites for calcium ions, until it was found that a subpopulation forms granules of a different type, which are used for heavy metal detoxification. Granules can be used in other ways as well. Certain polychaete worms, for example, strengthen their muscles by packing them with granules (Gibbs and Bryan 1984). Spicules are also commonly formed by many organisms and their functions are often not understood. They tend to have elaborate morphologies and mineralogies that are species specific, implying that they do perform specialized functions. These are just a few of many examples in which the functions of mineralized bodies still need to be determined. In this chapter we describe four different cases in which the functions are fairly well established. They have been investigated in some detail and, thus, provide good guidelines as to the various approaches by which function can be investigated. Some gravity receptors have been closely examined with respect to neuroanatomy and function, but not with respect to the specific adaptations of structure and mineralogy of the ubiquitous “heavy bodies.” Studies of biologic magnetic field receptors, in contrast, have focused on the mineral, and virtually nothing is known about the neuroanatomy. The molecular structure of the iron storage molecule ferritin is known with a resolution of a few Angstroms. Ferritin provides us with a glimpse of the insights that can be gained into function from such detailed structural information. Finally, some studies on the control of proteins on ice crystal formation represent the first application of the powerful techniques of molecular biology to determining function in biomineralization. These are undoubtedly the forerunners of many function-oriented studies using molecular biological techniques.
Conference papers on the topic "Intracellular Calcium Transient"
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Zhu, Geng, Wei Zhou, Yuan Zhang, Xiuli Liu, Yuxiang Wu, and Qingming Luo. "Application of confocal microscopy on glutamate-induced intracellular calcium transient in neurons." In Biomedical Optics 2006, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2006. http://dx.doi.org/10.1117/12.647145.
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Zhang, H., T. Tao, and S. C. O'Neill. "Approaching the mechanistic insights towards the genesis of intracellular calcium transient alternans - a simulation study." In 2008 35th Annual Computers in Cardiology Conference. IEEE, 2008. http://dx.doi.org/10.1109/cic.2008.4749069.
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Li, Wen, Miri Park, Catherine Kirn-Safran, Liyun Wang, and X. Lucas Lu. "Calcium Signaling of Chondrocytes Under Osmotic Stress and Mechanical Stimulation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80811.
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Chondrocytes play a critical role in cartilage remodeling by mediating the biosynthesis, organization, and modification of extracellular matrix (ECM) [1]. Previous studies showed that chondrocytes are highly sensitive to the surrounding mechanical and osmotic environments [2]. However, how these signals are perceived and transduced by chondrocytes remains unclear. One of the earliest responses of chondrocytes to stimuli is a transient oscillation in intracellular Ca2+ concentration ([Ca2+]i) [3]. The major objective of this study was to investigate and compare the Ca2+ signaling of chondrocytes, including both primary cells and chondrogenic cell line, under mechanical stimulus [4] and osmotic stress. The roles of seven essential pathways in Ca2+ signaling were further examined using pharmacological inhibitors.
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Enouf, J., R. Bredoux, A. Giraud, N. Bourdeau, and S. Levy-Toledano. "POSSIBLE RELATIONSHIP BETWEEN THE 23-kDa PHOSPHOPROTEIN AND THE IP3 -INDUCED Ca2+RELEASE IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644516.
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The regulation of Ca2+ concentration in human platelets involves intracellular membranes i.e. dense tubular system (DTS). Agonist-induced platelet activation generates inositol 1,4,5 trisphosphate (IP3) which is responsible for Ca2+ mobilization from DTS. However, its mechanism of action is still unknown. cAMP has been shown to regulate Ca2+ transport by isolated membrane vesicles. This effect was correlated with the phosphorylation of a 23 kDa protein. We investigated whether this phosphorylation could play a role in the mechanism of IP3-induced Ca release.We isolated a membrane fraction enriched in intracellular membranes, which actively sequesters Ca2++. The Ca2+ uptake was mediated by a characterized (Ca2+ + Mg2+)-ATPase of a molecular weight 120 kDa. As well, the characterization of the 23-kDa protein phosphorylation by the catalytic subunit of the cAMP dependent protein kinase (C. Sub.) has been achieved. IP^-induced Ca release was tested on our membrane preparations. The transient effect was maximal at one minute and a dose-response curve was obtained.The cAMP dependent phosphorylation of the 23-kDa protein increased the Ca2+ liberation induced by IP by two fold whatever the IP3 concentration. The addition on the protein kinase inhibitor inhibited the IP3 -induced Ca2+ release.The effect of IP3 on the cAMP-mediated phosphorylation of the 23-kDa protein has been examinated.A dose dependent stimu-ulation of the 23-kDa protein phosphorylation in the presence of C. Sub. was initiated by IP3. The maximal effect was observed after 1-2 min and obtained with an IP3 concentration similar to that producing the maximal calcium release. The stimulation of the phosphorylation by IP3 was detected in the absence of Ca2+ and in the presence of phosphatase inhibitors.Therefore, we suggest a possible correlation between cAMP dependent phosphorylation of the 23-kDa protein and the IP3-induced Ca2+ release in human platelet membrane vesicles.
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Sheikh, Abdul Q., Jennifer R. Hurley, and Daria A. Narmoneva. "Diabetes Alters Intracellular Calcium Transients in Cardiac Endothelial Cells." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53797.
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Diabetic cardiomyopathy (DCM) is a serious diabetes-associated complication that results in myocardial dysfunction independent of other etiological factors [1]. Pathological alterations to the myocardium associated with DCM include circulatory defects, impaired heart muscle contraction, and abnormal calcium (Ca2+) homeostasis in cardiac cells[2]. In myocardium, endothelial cells play an essential role in maintaining intracellular Ca2+ hemostasis in response to stimuli and regulating cardiac function [3]. External stimulus may cause abrupt changes in Ca2+ balance, including Ca2+ release from sarco-endoplasmic reticulum (ER) [4]. Subsequent return of the Ca2+ level to basal levels occurs due to Ca2+ decay mechanism, which is mainly regulated by sarco-endoplasmic reticulum Ca2+ ATPase pumps (SERCA) present at ER membrane which are responsible for Ca2+ sequestration [5]. Studies have shown that the mechanisms by which Ca2+ homeostasis alters cardiac function in diabetic cardiomyocytes include reduced activity of the SERCA pumps [6]. However, no information is available regarding the effects of diabetes on Ca2+ hemostasis and the underlying Ca2+ sequestration mechanism in diabetic cardiac endothelial cells[7]. This study tested the hypothesis that diabetic endothelial cells will exhibit disruptions in Ca2+ decay kinetics via alterations in the sequestration mechanism.
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Takayama, Yuzo, Akira Wagatsuma, Takayuki Hoshino, and Kunihiko Mabuchi. "Micropatterning C2C12 myotubes for orderly recording of intracellular calcium transients." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6611084.
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Lu, X. Lucas, Bo Huo, Andrew D. Baik, and X. Edward Guo. "Intercellular Calcium Wave Propagation in Linear and Circuit-Like Bone Cell Networks." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19365.
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Intracellular calcium ([Ca2+]i) transients in response to mechanical stimulation can be propagated to neighboring cells in bone cell networks, which provides an essential mechanism for cell-cell communication in bone. Transfer of intracellular second messengers (e.g., IP3 and Ca2+) through gap junction pores and the diffusion of extracellular ATP to activate membrane receptors have long been conjectured as the two major pathways for intercellular Ca2+ wave propagation [1]. In this study, by comparing the calcium wave in open-end linear and looped circuit-like cell chains, the roles of gap junction intercellular communication (GJIC) and extracellular ATP diffusion in calcium wave propagation in bone cell networks were examined. The results were further confirmed with pathway-inhibitor studies performed on linear cell chains.
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Lumbreras, V., E. Bas, C. Gupta, and S. M. Rajguru. "Pulsed Infrared-evoked Intracellular Calcium Transients in Neonatal Vestibular and Spiral Ganglion Neurons." In 2013 29th Southern Biomedical Engineering Conference (SBEC 2013). IEEE, 2013. http://dx.doi.org/10.1109/sbec.2013.59.
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Rink, T. J. "CALCIUM IN PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644772.
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Studies with calcium ionophores, permeabilised platelets, and platelets containing fluorescent calcium indicators quin2 and fura-2 have shown that elevation [Ca2+]i is an effective trigger for shape-change, aggregation, secretion and release of TxA2; and that elevation of [Ca2+]i is an important part of a complex “activation cascade” set up by natural agonists combining with their surface receptors. We have used calcium ionophores to impose [Ca2+]i changes, monitored by indicator dyes, to construct [Ca2+]i/function relationships for shape-change, secretion, aggregation, arachidonic acid release, TxA2 production, and myosin phosphorylation in intact platelets(e.g.1,2). Some of these functions can also be studied by analagous experiments using Ca2+-buffers to set known [Ca2+]i in permeabilised platelets. Our ability to monitor and modulate [Ca2+]i with fluorescent indicators has also allowed us to see what happens when [Ca2+]i changes are greately reduced or even absent and to investigate other pathways of intracellular activation. We think that formation of diacyl glycerol and activation of protein kinase-C can explain, some, but not all, of the cell activation that some agonists can apparently evoke at or near resting [Ca2+]i, and that combined or synergistic actions of Ca2+ and other intracellular mediators is the usual basis for physiological activation(3). Most agonists seem to promote both Ca2+ entry across the plasma membrahe and discharge from intracellular organelles, presumably the dense tubular system. The available evidence fits with the prevailing idea that Ins 1,4,5 P3 formed by agonist evoked hydrolysis of PIP2, is the internal messenger for Ca2+ release. Our kinetic measurements of [Ca2+]i transients require that optimal concentrations of InsP3 are formed within 250 milliseconds(4,5). The question of whether ADP receptors in human platelets are directly coupled with PIP2 breakdown remains contentious. Probably they do, weakly, and the differences from most other receptors are quantitative rather than qualitative. We do not understand the mechanisms of agonist-evoked Ca2+-entry; there is now plenty of evidence that argues against a role for membrane depolarisation and voltage-gated Ca channels, including some recent work with ionic substitution(5). Stopped-flow fluorescence analysis of [Ca2+]i rises in fura-2-loaded human platelets reveals some intriguing new insights(4,5). With thrombin, vasopressin and PAF at optimal concentrations, there is a highly reproducible delay before the signal starts to rise, which is approximately 250msec in the absence of external calcium compared to 190msec in the presence of external calcium. This suggests that Ca entry leads internal release, and gives ample time for complex coupling mechanisms for both processes.The delay with ADP, in the presence of external calcium, is much smaller suggesting a different coupling mechanism for Ca entry.
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McIntyre, Stephen D., Yoichiro Mori, and Elena G. Tolkacheva. "Local Onset of Voltage and Calcium Alternans in the Heart." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6148.
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A beat-to-beat variation in cardiac action potential durations (APD) is a phenomenon known as electrical alternans. Alternans desynchronizes depolarization, increases dispersion of refractoriness and creates a substrate for ventricular fibrillation. In the heart, APD alternans can be accompanied by alternans in intracellular calcium ([Ca2+]i) transients. Recently, we demonstrated experimentally that the onset of APD alternans in the heart is a local phenomenon that undergoes complex spatiotemporal dynamics as pacing rate increases. Moreover, the local onset of APD alternans can be predicted by measuring the restitution properties of periodically paced cardiac tissue. The purpose of this research is to investigate the interplay between local onsets of APD and [Ca2+]i alternans using 2D simulation of action potential model of cardiac myocytes.