Relevant bibliographies by topics / Calcium channel drugs

Academic literature on the topic 'Calcium channel drugs'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Calcium channel drugs"

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Triggle, David J. "Calcium-Channel Drugs." Journal of Cardiovascular Pharmacology 18 (1991): S1—S6. http://dx.doi.org/10.1097/00005344-199106191-00002.

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Triggle, David J. "Calcium-Channel Drugs." Journal of Cardiovascular Pharmacology 18 (1991): S1—S6. http://dx.doi.org/10.1097/00005344-199118101-00002.

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Triggle, David J. "Calcium, calcium channels, and calcium channel antagonists." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1474–81. http://dx.doi.org/10.1139/y90-224.

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Voltage-dependent Ca2+ channels are an important pathway for Ca2+ influx in excitable cells. They also represent an important site of action for a therapeutic group of agents, the Ca2+ channel antagonists. These drugs enjoy considerable use in the cardiovascular area including angina, some arrhythmias, hypertension, and peripheral vascular disorders. The voltage-dependent Ca2+ channels exist in a number of subclasses characterized by electrophysiologic, permeation, and pharmacologic criteria. The Ca2+ channel antagonists, including verapamil, nifedipine, and diltiazem, serve to characterize the L channel class. This channel class has been characterized as a pharmacologic receptor, since it possesses specific drug-binding sites for both antagonists and activators and it is regulated by homologous and heterologous influences. The Ca2+ channels of both voltage- and ligand-regulated classes are likely to continue to be major research targets for new drug design and action.Key words: calcium, calcium channels, calcium antagonists, 1,4-dihydropyridines, channel regulation, receptor regulation.
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MILLER-HANCE, WANDA C. "Calcium Channel-Blocking Drugs." Archives of Pediatrics & Adolescent Medicine 140, no. 12 (December 1, 1986): 1216. http://dx.doi.org/10.1001/archpedi.1986.02140260018012.

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CHO, CORNELIA. "Calcium Channel-Blocking Drugs-Reply." Archives of Pediatrics & Adolescent Medicine 140, no. 12 (December 1, 1986): 1216. http://dx.doi.org/10.1001/archpedi.1986.02140260018013.

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Schoenfeld, N., J. Aelion, Y. Beigel, O. Epstein, and A. Atsmon. "The porphyrogenic effects of calcium channel blocking drugs." Clinical Science 69, no. 5 (November 1, 1985): 581–86. http://dx.doi.org/10.1042/cs0690581.

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1. Treatment of monolayers of chick embryo hepatocytes with the calcium channel blocking drugs nifedipine and verapamil resulted in a decrease in the activity of uroporphyrinogen decarboxylase, an increase in the activity of δ-aminolaevulinate synthase and accumulation of porphyrins with uroporphyrin and heptacarboxylic porphyrin predominating. 2. Diltiazem, another calcium channel blocking drug, did not affect uroporphyrinogen decarboxylase activity and had a slight effect only on the accumulation of porphyrins. 3. Experiments with nifedipine and verapamil in the presence of various concentrations of calcium indicate that the porphyrogenic effect is apparently not related to blocking of calcium channels.
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White, Pamela. "Calcium Channel Blockers." AACN Advanced Critical Care 3, no. 2 (May 1, 1992): 437–46. http://dx.doi.org/10.4037/15597768-1992-2015.

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Calcium channel blockers are widely used in the treatment of ischemic heart disease, hypertension, and supraventricular tachycardia. The prototype agents, verapamil, nifedipine, and diltiazem, represent three classes of calcium channel blockers, each of which has different pharmacologic effects. Nifedipine and the other dihydropyridines primarily are vasodilators and have no clinical effects on cardiac conduction or contractility. Diltiazem and verapamil also are vasodilators, but they possess, to varying degrees, negative inotropic, chronotropic, and dromotropic effects. Side effects of these drugs are relatively rare and usually not serious, with the exception of potential conduction disturbances and heart failure in patients with underlying cardiac disease. To assess patients taking these medications and provide the necessary teaching, the nurse needs an understanding of the pharmacologic properties, clinical indications, and potential adverse effects of the various drugs
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Mogi, Masaki, and Masatsugu Horiuchi. "Calcium-Channel Blockers as Antidementia Drugs." Circulation Journal 80, no. 11 (2016): 2291–92. http://dx.doi.org/10.1253/circj.cj-16-0980.

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Nappi, Jean M., Jacqueline S. Marinac, and Patricia Bartlomé. "Calcium Channel Blockers." Journal of Pharmacy Practice 3, no. 5 (October 1990): 305–17. http://dx.doi.org/10.1177/089719009000300505.

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Calcium is an integral component in numerous physiological processes and functions. As such, drugs that interfere with the movement of calcium into or out of cells, or the activity of intracellular calcium are useful in treating a variety of disease states. This article will review the calcium channel blockers currently available, along with their approved indications, as well as select dihydropyridine investigational agents and nonapproved indications for their use.
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Ardizzone, Timothy D., Xiao-Hong Lu, and Donard S. Dwyer. "Calcium-independent inhibition of glucose transport in PC-12 and L6 cells by calcium channel antagonists." American Journal of Physiology-Cell Physiology 283, no. 2 (August 1, 2002): C579—C586. http://dx.doi.org/10.1152/ajpcell.00451.2001.

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The goal of these studies was to determine whether different calcium channel antagonists affect glucose transport in a neuronal cell line. Rat pheochromocytoma (PC-12) cells were treated with L-, T-, and N-type calcium channel antagonists before measurement of accumulation of 2-[3H]deoxyglucose (2-[3H]DG). The L-type channel antagonists nimodipine, nifedipine, verapamil, and diltiazem all inhibited glucose transport in a dose-dependent manner (2–150 μM) with nimodipine being the most potent and diltiazem only moderately inhibiting transport. T- and N-type channel antagonists had no effect on transport. The L-type channel agonist l-BAY K 8644 also inhibited uptake of 2-[3H]DG. The ability of these drugs to inhibit glucose transport was significantly diminished by the presence of unlabeled 2-DG in the uptake medium. Some experiments were performed in the presence of EDTA (4 mM) or in uptake buffer without calcium. The absence of calcium in the uptake medium had no effect on inhibition of glucose transport by nimodipine or verapamil. To examine the effects of these drugs on a cell model of a peripheral tissue, we studied rat L6 muscle cells. The drugs inhibited glucose transport in L6 myoblasts in a dose-dependent manner that was independent of calcium in the uptake medium. These studies suggest that the calcium channel antagonists inhibit glucose transport in cells through mechanisms other than the antagonism of calcium channels, perhaps by acting directly on glucose transporters.
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Dissertations / Theses on the topic "Calcium channel drugs"

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Young, Lois-May. "Evaluation of polycyclic amines as modulators of calcium homeostasis in models of neurodegeneration / Young L." Thesis, North-West University, 2012. http://hdl.handle.net/10394/7591.

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Compromised calcium homeostasis in the central nervous system (CNS) is implicated as a major contributor in the pathology of neurodegeneration. Dysregulation of Ca2+ homeostasis initiates downstream Ca2+–dependent events that lead to apoptotic and/or necrotic cell death. Increases in the intracellular free calcium concentration ([Ca2+]i) may be the result of Ca2+ influx from the extracellular environment or Ca2+ release from intracellular Ca2+ stores such as the endoplasmic reticulum (ER). Influx from the extracellular environment is controlled predominantly by voltage gated calcium channels (VGCC), such as L–type calcium channels (LTCC) and ionotropic glutamate receptors, such as the N–methyl–D–aspartate (NMDA) receptors. Ca2+ release from the ER occurs through the inositol–1,4,5–triphosphate receptors (IP3Rs) or ryanodine receptors (RyRs) via IP3–induced or Ca2+–induced mechanisms. Mitigation of Ca2+ overload through these Ca2+ channels offers an opportunity for pharmacological interventions that may protect against neuronal death. In the present study the ability of a novel series of polycyclic compounds, both the pentacycloundecylamines and triquinylamines, to regulate calcium influx through LTCC was evaluated in PC12 cells using calcium imaging with Fura–2/AM in a fluorescence microplate reader. We were also able for the first time to determine IC50 values for these compounds as LTCC blockers. In addition, selected compounds were evaluated for their ability to offer protection in apoptosis–identifying assays such as the lactate dehydrogenase release assay (LDH–assay), trypan blue staining assay and immunohistochemistry utilizing the Annexin V–FITC stain for apoptosis. We were also able to obtain single crystal structures for the tricyclo[6.3.0.02,6]undecane–4,9–dien–3,11–dione (9) and tricyclo[6.3.0.02,6]undecane–3,11–dione (10) scaffolds as well as a derivative, N–(3–methoxybenzyl)–3,11–azatricyclo[6.3.0.02,6]undecane (14f). We also evaluated the possibility that the polycyclic compounds might be able to modulate Ca2+ flux through intracellular Ca2+ channels. Computational methods were utilized to accurately predicted IC50 values and develop a QSAR model with marginal error. The linear regression model delivered r2 = 0.83, which indicated a favorable correlation between the predicted and experimental IC50 values. This model could thus serve as valuable predictor for future structural design and optimization efforts. Data obtained from the crystallographic analysis confirmed the NMR–data based structural assignments done for these compounds in previous studies. Obtaining structural information gave valuable insight into the differences in size and geometric constrains, which are key features for the LTCC activity of these compounds. vii In conclusion, we found that all of the compounds evaluated were able to attenuate Ca2+ influx through the LTCC, with some compounds having IC50 values comparable with known LTCC blockers such as nimodipine. Representative compounds were evaluated for their ability to afford protection against apoptosis induced by 200 ?M H2O2. With the exception of compound 14c (the most potent LTCC blocker in the series, IC50 = 0.398 ?M), most compounds were able to afford protection at two or more concentrations evaluated. Compound 14c displayed inherent toxicity at the highest concentrations evaluated (100 ?M). We concluded that compounds representing both types of structures (pentacycloudecylamines and triquinylamines) have the ability to attenuate excessive Ca2+ influx through the LTCC. In general the aza–pentacycloundecylamines (8a–c) were the most potent LTCC blocker which also had the ability to offer protection in the cell viability assays. However, NGP1–01 (7a) had the most favorable pharmacological profile overall with good activity as an LTCC blocker (IC50 = 86 ?M) and the ability to significantly attenuate cell death in the cell viability assays, exhibiting no toxicity. In addition to their ability to modulate Ca2+ influx from the extracellular environment, these compounds also displayed the ability to modulate Ca2+ flux through intracellular Ca2+ channels. The mechanisms by which they act on intracellular Ca2+ channels still remains unclear, but from this preliminary study it would appear that these compounds are able to partially inhibiting Ca2+–ATPase activity whilst possibly simultaneously inhibiting the IP3R. In the absence of extracellular Ca2+ these compounds showed the ability in inhibit voltage–induced Ca2+ release (VICaR), possibly by modulating the gating charge of the voltage sensor being the dihydropyridine receptors. In future studies it might be worthwhile to do an expanded QSAR study and evaluate the aza–pentacycloundecylamines. To clarify the mechanisms by which the polycyclic compounds interact with intracellular Ca2+ channels we should examine the direct interaction with the individual Ca2+ channels independently. The polycyclic compounds evaluated in this study demonstrate potential as multifunctional drugs due to their ability to broadly regulate calcium homeostasis through multiple pathways of Ca2+ entry. This may prove to be more effective in diseases where perturbed Ca2+ homeostasis have devastating effects eventually leading to excitotoxicity and cell death.
Thesis (Ph.D. (Pharmaceutical Chemistry))--North-West University, Potchefstroom Campus, 2012.
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Zhang, Changfeng. "Investigation of the endoplsmic reticulum calcium stores for their potential roles in neuroprotection using the NG115-401L neuronal cell line model." Scholarly Commons, 2014. https://scholarlycommons.pacific.edu/uop_etds/142.

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There is significant interest in the field of neuroscience to gain a better understanding of how neurons die in neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. We have used the neuronal cell line NG115-401L with unique calcium signaling characteristics to test the hypothesis that improving calcium loading into the endoplasmic reticulum (ER) to increase ER calcium levels acts as a possible neuroprotective response. We approached this problem using both pharmacological and genetic approaches targeting the central mediator of calcium uptake in the ER localized sarco/endoplasmic reticulum Ca 2+ ATPase (SERCA) enzyme. The pharmacological studies involved use of the ginger root compound 6-gingerol, which to date is the best documented agent for activating SERCA enzymes in heart and skeletal muscle. However, in our experiments, gingerol did not appear to activate NG115-401L SERCA pumps; indeed, the compound produced a response more like that of a SERCA inhibitor inducing a rapid ER calcium depletion. In addition, gingerol stimulated robust calcium influx responses, an unexpected result given the NG115-401L neural cell line is uniquely deficient in calcium influx pathways. Our genetic approach involved expressing the stromal interaction molecule 1 (STIM1) protein in the NG115-401L cell, which is also an ER localized protein that serves as a pivotal calcium influx channel regulator. NG115-40lL neurons present a native deficiency of STIM1 expression in a background phenotype with well characterized perturbations in ER calcium regulation and control of calcium influx pathways. Thus, STIM1 may be predicted to increase ER calcium levels, conferring protection against neuron cell death due to ER calcium store defects. STIM1 expression reconstituted the corrupted calcium influx pathway in NG115-401L neurons, which conferred neuroprotective responses to ER calcium perturbation, mitochondrial oxidative stress and subsequent cell death. Our results argue for unique and undiscovered regulatory effects of gingerol on the ER calcium circulation system, and suggest that the expression of STIM1 in these neurons protects against ER stress and oxidative stress via reconstruction of cellular calcium homeostasis.
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Ruchala, Iwona. "EXPANDING MONOAMINE TRANSPORTERS PHARMACOLOGY USING CALCIUM CHANNELS." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/5032.

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Research in drug development meets many challenges including lengthy, complex and costly procedures to identify novel pharmacotherapies. In our lab, we developed a method for fast screening of small molecules that interact with monoamine transports – dopamine and serotonin (DAT, SERT). These membrane proteins play important roles in brain neurotransmission responsible for cognition, motion and pleasure. Dysfunction in dopaminergic and serotonergic systems result in neurological disorders such as depression, Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia and addiction. DAT and SERT are responsible for uptake of dopamine (DA) or serotonin (5HT) into the synapse and they limit neurotransmitter signaling. Drugs that mimic or antagonize actions of endogenous neurotransmitters (DA and 5HT) increase the concentrations of DA and/or 5HT either by blocking the transporter (blockers) or by competing uptake with neurotransmitter (substrate). The uptake of substrates is associated to an inward current that depolarizes the cell membrane. Voltage-gated calcium channels (CaV) can respond to small changes in membrane potential. In our method, we combined permanent cell line expressing the human dopamine transporter (hDAT) or the human serotonin transporter (hSERT) (FlpIn TREx expression system) with transient transfection of CaV. This system works as a tightly electrically coupled system. Cells challenged with substrate of the transports produce detectable Ca2+ signal while monoamine transporter blockers can inhibit these Ca2+ signals. The novelty of this method relies on the ability to discriminate between substrate and blockers of monoamine transporters. Preliminary experiments measuring our optimized cell system in a Flex Station 3 plate reader suggest that the co-expression of a voltage-gated Ca2+ channel, a monoamine transporter and a genetically encoded Ca2+ sensor constitute a rapid screening biosensor to identify active drugs at monoamine transporters. Our novel methodology can rapidly assess drug-effect profile on monoamine transporters and benefit development of new psychotherapeutics for treatment of mental illnesses. It can also be used to characterize mechanism of action of emerging drug of abuse, as well as to discover small molecules with novel drug-effect profile useful in basic neuroscience research.
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Dowell, Margaret Anne. "Influence of three-tier cost sharing on patient compliance with and switching of cardiovascular medications." Columbus, Ohio : Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1030118543.

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Thesis (M.S.--Ohio State University, 2002.
Title from first page of PDF file. Document formatted into pages; contains xvi, 173 p.: ill. Includes abstract and vita. Co-advisors: Craig A. Pedersen, Dept. of Pharmacy; Anne Scheck McAlearney, School of Public Health. Includes bibliographical references (p. 169-173).
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Herzinger, Thomas Andreas. "Effects of the Cardioprotective Drugs Dexrazoxane and ADR-925 on Doxorubicin Induced Ca2+ Release from the Sarcoplasmic Reticulum." PDXScholar, 1996. https://pdxscholar.library.pdx.edu/open_access_etds/5069.

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The sarcoplasmic reticulum is the intramuscular organelle responsible for the regulation of cytoplasmic calcium levels in muscle. This thesis investigates the effects of the cardioprotective drug, dexrazoxane, and its metabolite ADR-925 on doxorubicin induced calcium release from skeletal sarcoplasmic reticulum. Doxorubicin is a widely used antineoplastic agent. One of the major side effects of doxorubicin usage is chronic cardiotoxicity. Doxorubicin is a potent activator of the calcium release mechanism from the SR. The interaction between doxorubicin and the calcium release channel has been proposed as the possible underlying mechanism behind cardiotoxicity. A short overview of different hypotheses describing doxorubicin induced cardiotoxicity and proposed mechanisms of cardioprotection by dexrazoxane are presented. While dexrazoxane did not appear to affect the calcium permeability of the SR, its metabolite, ADR-925, modulates the ryanodine receptor complex. ADR-925 inhibits high affinity ryanodine binding to the ryanodine receptor/calcium release channel complex by decreasing the sensitivity of the receptor for stimulation by calcium. ADR-925's ability to inhibit doxorubicin stimulated ryanodine binding is independent of the doxorubicin concentration. These results demonstrate that ADR-925 directly affects the ryanodine receptor complex of the SR by desensitizing the receptor to activation by calcium. Furthermore, ADR-925 reduces the inhibitory effect of hydrogen peroxide on the ryanodine receptor/ calcium release channel. This suggests that ADR-925 may protect the SR from oxidative effects of free radicals. It has been somewhat controversial whether doxorubicin induced cardiotoxicity is due to a specific interaction with the calcium release mechanism of SR. The findings presented in this thesis which demonstrate that the cardioprotectant ADR-925 interacts directly with the ryanodine receptor from SR, further support the hypothesis that the ryanodine receptor is a primary target of doxorubicin's action.
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Whittington, Miles A. "The ethanol withdrawal syndrome : a role for dihydropyridine-sensitive calcium channels in neural hyperexcitability states." Thesis, University of Bristol, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279774.

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Brown, Jason Peter. "The novel antiepileptic drug, gabapentin (Neurontin), binds to the α₂δ subunit of a voltage-dependent calcium channel." Thesis, University of Cambridge, 1996. https://www.repository.cam.ac.uk/handle/1810/252157.

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Florent, Romane. "Intérêt de la modulation pharmacologique des voies de signalisation calcique pour restaurer le contrôle de l'apoptose dans les cancers ovariens chimiorésistants Inhibition of store-operated channels by carboxyamidotriazole sensitizes ovarian carcinoma cells to anti-BclxL strategies through Mcl-1 down-regulation Drug Repositioning of the α1-Adrenergic Receptor Antagonist Naftopidil: A Potential New Anti-Cancer Drug? Bim, Puma and Noxa upregulation by Naftopidil sensitizes ovarian cancer to the BH3-mimetic ABT-737 and the MEK inhibitor Trametinib." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC413.

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Le sombre pronostic du cancer de l’ovaire s’explique notamment par une fréquence importante de résistance à la chimiothérapie conventionnelle présentée par les patientes. La mise en place de stratégies thérapeutiques alternatives à la chimiothérapie, mais aussi la découverte de biomarqueurs prédictifs de la réponse à ce traitement, représentent donc un enjeu majeur pour améliorer la prise en charge de cette pathologie. La chimiorésistance des cellules cancéreuses ovariennes s’explique principalement par leur résistance à l’apoptose, résultant d’un déséquilibre entre les membres pro- et anti-apoptotiques de la famille Bcl-2 qui contrôlent cette mort cellulaire. De ce fait, toutes stratégies capables de moduler le ratio [pro ]/[anti apoptotiques] en faveur des [pro-] restaure efficacement l’apoptose de ces cellules. Or, la signalisation calcique est connue pour réguler l’expression de ces protéines et apparait ainsi comme une cible pertinente pour restaurer l’apoptose des cellules cancéreuses ovariennes chimiorésistantes. Dans ce contexte, nous avons mis en évidence que trois modulateurs du signal calcique sont capables d’induire la mort de ces dernières en association à l’ABT-737, un BH3-mimétique ciblant l’activité de l’anti apoptotique Bcl-xL. Cette sensibilisation à l’ABT-737 est permise par le fait que le carboxyamidotriazole réprime l’expression de l’anti apoptotique Mcl-1 via l’inhibition des courants SOCE, le naftopidil augmente l’expression des protéines pro apoptotiques via l’induction d’un stress du RE ou l’activation de JNK et que la thapsigargine semble préparer à la mort cellulaire grâce à une augmentation de la concentration calcique intracellulaire via STIM1 et, peut-être, via l’induction de l’expression de Noxa. En outre, les acteurs de la signalisation calcique, connus pour subir un remodelage au cours des processus de cancérogenèse pourraient se révéler comme des outils de prédiction de réponse à la chimiothérapie. Dans ce contexte, nous avons mis en évidence que l’expression de la pompe calcique SERCA2 semble jouer le rôle de biomarqueur prédictif de la réponse à la chimiothérapie des patientes atteintes d’un cancer de l’ovaire
The poor prognosis of ovarian cancer is mainly explained by a high rate of resistance to conventional chemotherapy presented by patients. Therefore, discovery of both alternative therapeutic strategies to chemotherapy and predictive biomarkers for response to this treatment represent a major challenge for improving the management of this pathology. Chemoresistance of ovarian cancer cells is mainly due to their resistance to apoptosis, resulting from an imbalance between the pro- and anti-apoptotic members of the Bcl-2 family that control this type of cell death. Thus, all strategies able to modulate the [pro]/[anti-apoptotic] protein ratio in favor of [pro-] effectively restore apoptosis in these cells. However, calcium signaling is known to regulate the expression of these proteins and thus appears to be a relevant target for restoring apoptosis in chemoresistant ovarian cancer cells. In this context, we have shown that three calcium signal modulators are able to induce the death of these cells in association with ABT-737, a BH3-mimetic targeting the activity of the anti-apoptotic Bcl-xL. This sensitization to ABT-737 is enabled by the fact that carboxyamidotriazole represses the expression of the anti apoptotic Mcl-1 via the inhibition of SOCE currents, naftopidil increases pro-apoptotic protein expression via ER stress induction or JNK activation and thapsigargin seems to prepare cell death through increasing intracellular calcium concentration via STIM1 and, maybe, through Noxa expression induction. In addition, players of the calcium signaling toolkit, known to undergo remodeling during carcinogenesis could be proven as tools for predicting response to chemotherapy. In this context, we have shown that the expression of the calcium pump SERCA2 seems to play a role as a predictive biomarker for response to chemotherapy of patients with ovarian cancer
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Olah, Mark E. "Effects of calcium channel blockade and intracellular calcium antagonism on endothelium-dependent responses of the isolated rat aorta and influence of the endothelium on drug action /." The Ohio State University, 1988. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487590702989006.

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Zhang, Yi. "Potential impact of breast cancer resistance protein on drug disposition during pregnancy /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/7970.

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Books on the topic "Calcium channel drugs"

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Opie, Lionel H. Clinical use of calcium channel antagonist drugs. Boston: Kluwer Academic Publishers, 1989.

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Opie, Lionel H. Clinical use of calcium channel antagonist drugs. 2nd ed. London: Kluwer, 1990.

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Opie, Lionel H., and William A. Coetzee. Clinical Use of Calcium Channel Antagonist Drugs. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0863-8.

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Japan-U.S.A. Symposium on Cardiovascular Drugs (1989 Kahuku, Hawaii). Recent advances in calcium channels and calcium antagonists: Proceedings of the Japan-U.S.A. Symposium on Cardiovascular Drugs. Edited by Yamada Kazuo and Shibata Shoji. New York: Pergamon Press, 1990.

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Drugs looking for diseases: Innovative drug research and the development of the beta blockers and the calcium antagonists. Dordrecht: Kluwer Academic Publishers, 1991.

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Albrecht, Fleckenstein, ed. Cardiovascular effects of dihydropyridine-type calcium antagonists and agonists. Berlin: Springer-Verlag, 1985.

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Godfraind, T. Calcium channel blockers. Boston, MA: Birkhauser Verlag, 2003.

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Calcium channel blockers. Basel: Birkhäuser Verlag, 2004.

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S, Meldrum Brian, Williams, Michael, 1947 Jan. 3-, and Princeton Drug Research Symposia (1st : 1989 : Princeton, N.J.), eds. Current and future trends in anticonvulsant, anxiety, and stroke therapy: Proceedings of a symposium held at Princeton, New Jersey, May 21-23, 1989. New York: Wiley-Liss, 1990.

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Roberto, Robles Nicolás, ed. Calcium channel blockers and renal disease. Hauppauge, NY: Nova Science Publishers, 2009.

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Book chapters on the topic "Calcium channel drugs"

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Özkaya, Esen, and Kurtuluş Didem Yazganoğlu. "Calcium Channel Blockers." In Adverse Cutaneous Drug Reactions to Cardiovascular Drugs, 129–42. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6536-1_8.

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Tülümen, Erol, and Martin Borggrefe. "Modulation of Calcium Handling: Calcium-Channel Modulators." In Antiarrhythmic Drugs, 233–64. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-34893-9_5.

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Merin, R. "Calcium Channel Blocking Drugs: New Developments." In Anesthesiology and the Heart, 119–23. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1966-2_13.

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Doyle, Austin E. "Calcium Channel Blocking Drugs as Antihypertensive Agents." In International Yearbook of Nephrology 1989, 89–113. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1673-2_5.

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Coetzee, William A. "Channel-Mediated Calcium Current in the Heart." In Clinical Use of Calcium Channel Antagonist Drugs, 1–27. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0863-8_1.

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Herbette, Leo G., Giovanni Gaviraghi, Robert J. Dring, Lawrence J. Briggs, and R. Preston Mason. "Interactions of Lacidipine and other Calcium Channel Drugs with Biological Membranes: A Structural Model for Receptor/Drug Binding Utilizing the Membrane Bilayer." In Calcium Antagonists, 15–23. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1725-8_3.

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Opie, Lionel H., and William A. Coetzee. "Fundamental Properties: Mechanisms, Classification, Sites of Action." In Clinical Use of Calcium Channel Antagonist Drugs, 28–69. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0863-8_2.

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Opie, Lionel H., and William A. Coetzee. "Use and Comparative Properties of the Three Prototypical Calcium Antagonists in Ischemic Heart Disease, Including Recommendations Based on an Analysis of 41 Trials." In Clinical Use of Calcium Channel Antagonist Drugs, 70–130. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0863-8_3.

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Opie, Lionel H., and William A. Coetzee. "Use and Comparative Efficacy in Hypertension and Supraventricular Arrhythmias. Minor Indications." In Clinical Use of Calcium Channel Antagonist Drugs, 131–92. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0863-8_4.

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Opie, Lionel H., and William A. Coetzee. "Side Effects and Contraindications Drug Interactions and Combinations." In Clinical Use of Calcium Channel Antagonist Drugs, 193–218. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0863-8_5.

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Conference papers on the topic "Calcium channel drugs"

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Kakariqi (Pepa), Laerta, and Sonila Vito. "Utilization of vascular calcium channel blocker drugs in Primary Health Care in Albania during 2004-2014." In The 5th Virtual International Conference on Advanced Research in Scientific Areas. Publishing Society, 2016. http://dx.doi.org/10.18638/arsa.2016.5.1.815.

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Yalcin, Huseyin C., Mohamed A. Elrayess, Hadeel T. Al-Jighefee, Mahmoud Khatib A. A. Al-Ruweidi, Shamma Almuraikhy, and Hadi M. Yassine. "Soluble ACE2 and Angiotensin II levels Modulated in Hypertensive COVID-19 Patients treated with different Antihypertension Drugs." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0085.

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Hypertension is a major risk factor and common comorbidity among severe Coronavirus Disease 2019 (COVID-19) patients. Prominent antihypertensive drugs, such as angiotensin-converting-enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB) can modulate the expression of angiotensin-converting enzyme 2 (ACE2) and may influence COVID-19 prognosis. Other classes of antihypertensive drugs, such as beta-blockers (BB) and calcium channel blockers (CCB) are associated with reduced mortality. Still, their effect on the circulating levels of ACE2 and angiotensin II, as well as the severity of COVID-19, are less characterized. Two hundred hypertensive COVID-19 patients on four different classes of antihypertensive medication (ACEi, ARB, BB, and CCB), with different COVID-19 severities (mild, moderate, and severe) were recruited, and clinical data were assessed. Sera-circulating ACE2 and angiotensin II levels were measured using standard ELISA kits. Linear regression models were used to assess the effect of antihypertensive medications on circulating levels of ACE2 and angiotensin II in relation to disease severity and other clinical indices. Included patients were on ACEi (n=57), ARB (n=68), BB (n=15), or CCB (n=30), with mild (n=76), moderate (n=76), or severe (n=52) COVID-19. ACE2 levels were higher in patients with severe COVID-19 than those with mild (p=0.04) and moderate (p=0.007) disease. ACE2 levels correlated positively with the length of hospital stay (r=0.3, p=0.003), while angiotensin II levels decreased with disease severity (p=0.04). Higher ACE2 levels were associated with elevated CRP and D-dimer, while higher angiotensin II levels were associated with lower levels of CRP, D-dimer, and troponin. Among the four treated groups, patients on ARB exhibited elevation in ACE2 levels with increased disease severity (p=0.01), whereas patients on ACEi showed lower angiotensin II levels with increased disease severity. Patients on BB showed the lowest disease severity compared to other treated groups. Our data show increased COVID-19 severity with elevated levels of circulating ACE2 and lower levels of angiotensin II and suggest a protective effect of BB treatment against disease severity in hypertensive patients, independently of ACE2 and angiotensin II levels.
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Krasnoshtanova, Alla, and Anastasiya Bezyeva. "DETERMINATION OF THE OPTIMAL CONCENTRATIONS OF PECTIN AND CALCIUM CHLORIDE FOR THE SYNTHESIS OF CHITOSAN-PECTIN MICROPARTICLES." In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/09.

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"The oral route of drug inclusion is the most convenient for the patient. In addition to ease of use, this method of drug inclusion has such advantages as non-invasiveness of inclusion, absence of complications during injection; comparative safety for the organism due to the passage of the active substance and auxiliary compounds through the gastrointestinal tract; the possibility of introducing larger doses of the drug at one time. However, despite the obvious advantages, the oral route of inclusion has a number of significant disadvantages that significantly limit its use for a number of drugs. Among them are: relatively slow therapeutic action of the drug with this route of inclusion; the aggressive effect of a number of drugs (for example, antibiotics) on the gastrointestinal tract; low bioavailability of a number of substances (especially high molecular weight hydrophilic compounds), caused by poor permeability of the intestinal epithelium for hydrophilic and large molecules, as well as enzymatic and chemical degradation of the active substance in the gastrointestinal tract. There are various approaches used in the development of oral drug delivery systems. In particular, for the targeted delivery of drugs, it is proposed to use nano- and microcapsules with mucoadhesive properties. Among the polymers used for the synthesis of these microparticles, it is preferable to use pH-dependent, gelable biopolymers that change their structure depending on the acidity of the environment. Microcapsules obtained from compounds with the above properties are capable of protecting the active substance (or from the active substance) in the stomach environment and ensuring its release in the intestine. These properties are possessed by such polysaccharides as alginate, pectin, carrageenan, xylan, etc. The listed biopolymers are non-toxic, biocompatible, and biodegradable, which makes microparticles containing these polysaccharides promising as oral drug delivery systems. To impart mucoadhesive properties to nanoparticles, complexes of the listed polymers with chitosan are used. In this research, pectin, a polysaccharide formed mainly by residues of galacturonic acid, was used as a structural polymer. The concentrations of substances in the initial solutions were selected that were optimal for the synthesis of microcapsules. The main parameters for evaluating the resulting microparticles were the size of the capsules (less than 1 μm for oral inclusion), the zeta-potential, showing the tendency of the microparticles to stick together, and the completeness of the binding of the microparticles to chitosan. It was found that the optimal solutions for the synthesis of microparticles are: 15.7 ml of a solution of pectin 0.093% by weight, 3.3 ml of a solution of chitosan 0.07% by weight and 1.0 ml of a solution of CaCl2 20 mM. The diameter of the microparticles obtained by this method was 700-800 nm, and the value of their zetta-potential, equal to - (34 ± 3) mV, does not cross the particle adhesion threshold. It was also found that the synthesis of microparticles at these concentrations of calcium chloride provides the most complete binding of chitosan to their surface, which increases the mucoadhesive properties of microparticles."
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Silva, Vitoria Pimentel da, Laura Provenzi, Nicole Becker, Giovani Zocche, Gabriel Leal, Giulia Pinzetta, Allan Alcará, et al. "Mesenchymal stem cells modulate the gene expression of T- type Calcium Channel Subunit Alpha 1G (Cav3.1) in acute phase of epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.709.

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Introduction: Temporal Lobe Epilepsy (TLE) is a disorder caused by neuronal electrical imbalance, clinically manifested by spontaneous and recurrent seizures1,2. Its pathogenesis involves channelopathies of calcium channels, which contributes to hyperexcitability and hypersynchrony in TLE3 . About 30% of patients do not respond to drug treatment4 , making it necessary to develop new therapeutic alternatives, such as cell therapy. This work aimed to evaluate the modulation of mesenchymal stem cells (MSCs) in the calcium channel CACNA1G (Cav3.1) gene expression. Methods: MSCs were extracted from Wistar rats bone marrow and then cultured and transplanted intravenously and intranasally in the control and epileptic groups. The brain was collected 1 and 7 days after transplantation to analyze gene expression. Results: The analysis showed that treated animals had greater gene expression, compared to animals not treated in the epileptic and control group, in both days and administration routes. Furthermore, epileptic animals that were not treated had a low or negative expression of the gene. The epileptic rats that were treated, on the other hand, had a marked increase in gene expression e in the prefrontal cortex. Conclusion: This up-regulation noted on the treated groups raises the hypothesis that MSCs would be using these channels to modify the microenvironment5 , intensifying Cav.3.1 transcription and contributing to tissue regeneration by neurodifferentiation6,7. This is supported by the increase in the calcium influx present in the early stages of neuronal maturation8,9. Thus, MSCs can modulate gene expression in the pilocarpine-induced animal’s brain, making Cav3.1 a target to be explored in epilepsy.
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Vaibavi, S. R., Rahul Vaippully, Basudev Roy, and Saumendra K. Bajpai. "Anti-hypertensive Calcium-Blocking Drugs Induce a Change in Viscoelasticity of Mcf-7 Cancer Cells." In ICBET 2020: 2020 10th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3397391.3397420.

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Souza, Isabela Silva, Beatriz Cassarotti, Lucas de Oliveira Pinto Bertoldi, Alana Strucker Barbosa, Eduardo Silveira Marques Branco, Isabela Badan Fernandes, Bruno Eji Nakano, et al. "Fahr syndrome associated with post-thyroidectomy hypoparathyroidism." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.567.

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Context: Fahr’s syndrome is a rare disorder characterized by bilateral and symmetrical abnormal calcifications in basal ganglia and cerebral cortex. Those calcified deposits are due to changes in calcium and phosphorus metabolisms that can be caused by endocrine disorders, mitochondrial myopathies, dermatological and infectious diseases. Clinical manifestations may include a variety of extrapyramidal, cerebelar and neuropsychiatric syndromes. Case report: This study describes a 75-year-old female patient that underwent total thyroidectomy in 1985 due to a multinodular goiter and presented postsurgical hypoparathyroidism. The patient missed follow-up apppoointments with Endocrinology and stopped treating her parathyroid condition. Some time later, she presented with change in behavior, drowsiness, paraesthesias, limb spasms and seizures. A CT scan of the brain was performed, showing multiple and extensive calcifications reaching the cerebellar hemispheres, basal ganglia, thalamus and white subcortical substance symmetrically. Laboratory examinations revealed hypocalcemia, hyperphosphatemia, and low parathyroid hormone (PTH) levels. Intravenous calcium gluconate was used to corret the Ca/P dysfunction. Additionally, appropriate antiepileptic drugs for seizures were used. She presented with progressive improvement of symptoms after treatment. Conclusions: This case report demonstrates the importance of post- thyroidectomy follow-up and early recognition of Fahr syndrome’s symptoms, which prevents the progression of neurological conditions.
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Patil, Vaishali, and Neeraj Masand. "Applications of Structure Based Drug Design Approaches towards Design and Development of Calcium Channel Blockers." In MOL2NET 2017, International Conference on Multidisciplinary Sciences, 3rd edition. Basel, Switzerland: MDPI, 2017. http://dx.doi.org/10.3390/mol2net-03-05051.

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Wang, C. T., J. Y. Lee, J. C. Chen, Y. J. Shiao, and W. J. Tsai. "EFFECT OF TRIFLUOPERAZINE (TFP) ON HUMAN PLATELET MEMBRANE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644816.

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TFP is a lipophilic antipsychotic drug. The drug will first encounter with cell membrane when adding it into a cell suspension. The effect of TFP on plasma membrane of the gel-filtered human platelet was investigated by : 1) scanning electron microscopy (SEM); 2) measuring theleakiness of marker enzymes and compound; 3) estimating its solubility in membrane. The cells were suspended in the modified Tyrode's buffer containing 0.1% dextrose, 0.2% of bovine serum albumin and without calcium. The SEM study showed that platelet changed shape from disc to ellipsoid in 10 μM TFP.,Increasingthe TFP concentration from 20 μM to 50 μM resulted in changing thecell from ellipsoid to sphere with a wavy surface. The drug did not cause any significant change in the cell volume. TFPof 70 μM caused platelet becoming a round ball shape with a spongy-like cell surface. 100 μM TFP caused more than 90% of cells to lyse and to agglutinate with each other. The time courseof morphological change of the TFP-affected platelets showed that the cellsswelled into irregular shape within 2 min. Apparent leakiness of serotonin was observed at 20 μM TFP, while the leakages of both lactate dehydrogenase and acid hydrolase were found at 40 μM TFP. The TFP uptake study showed that platelet was permeable to TFP by simple diffusion. The partition coefficient of TFP in platelet membrane was estimated to be 1 x 104. These results indicate that TFP molecules are solubilized in membrane. The extent in perturbation of the membrane structure depends on concentration of the drug used. (This research was supported by a grant from the National Science Council of the Republic of China.)
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Nagata, H., S. Nomura, K. Oda, T. Kokawa, and K. Yasunaga. "ANALYSIS OF THE FUNCTIONAL ROLE OF PLATELET MEMBRANE GLYCOPROTEINS WITH MONOCLONAL ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643509.

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Eight monoclonal antibodies were obtained which recognized platelet surface antigens of these, 5 (NNKYl-32, NNKY2-5, NNKY2-6, NNKY2-11, NNKY2-18 ) recognized GP IIb-IIIa complex, 2 (NNKY5-4, NNKY5-5 ) recognized GP lb and 1 (NNKYl-19) recognized CD 9 antigen. They were used to research the platelet membrane antigens.Monoclonal antibodies that recognize CD 9 antigen, which exists on the surface of platelets, acute lymphoblastic leukemia cells, eosinophils and other tissue, are known to act as an aggregating agent to platelets and NNKYl-19 was fond to induce platelet aggregation accompanied by ATP release. NNKY5-4 had no effect on platelet functions. NNKY5-5 inhibited aggregation induced by ristocetin but had no effect on aggregation induced by ADP, collagen, thrombin, and NNKYl-19. NNKYl-32, 2-5, 2-6, 2-11, and 2-18 inhibited aggregation induced by ADP, collagen, thrombin, and NNKYl-19, although slight release of ATP was recognized when NNKYl-19-induced aggregation was completely inhibited by NNKYl-32. Mutual inhibition of binding to platelet membranes between the 3 groups of monoclonal antibodies was not recognizedNNKYl-19-induced aggregation was associated with a lag time that was plo-longed in inverse proportion to antibody concentration. Aspirin had almost no effect on NNKYl-19-induced aggregation. A TXA2 receptor antagonist, a calci-um-channel blocking drug and EDTA inhibited NNKYl-19-induced aggregation. These results indicate that GP I b, GP IIb-IIIa complex and the cyclooxygenase pathway are not involved in NNKYl-19-induced platelet activation, that the target of NNKYl-19 on the platelet membrane is same as that of TXA2, and that the mechanism of activation by NNKYl-19 is related to calcium flux.
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SIMON, M. F., H. CHAP, and L. DOUSTE-BLAZY. "EFFECTS OF SIN 1 ON PLATELET ACTIVATION INDUCED BY THROMBIN IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643423.

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The mechanism of platelet activation is well known. The interaction of agonist such as thrombin, on specific membrane receptor induces phosphatidylinositol-specific phospholipase C activation, with a concomitant formation of two second messengers (from PIP2): inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 is able to induce a rapid discharge of Ca2+ from internal stores and Ca2+ influx through plasma membrane by unidentified Ca2+ channels linked to receptor activation. The increase of cytoplasmic free calcium concentration leads to the activation of the calcium calmodulin dependent myosine light chain kinase which phosphoryla-tes 20 kD proteins (myosine light chain). DAG is a potent activator of protein kinase C, which phosphorylates 40 kD proteins. These different pathways act in synergism.Sin 1 is a platelet aggregating inhibitor. This compound is an active metabolite of molsidomine, which activates platelet guany-late cyclase, inducing a rapid rise in cyclic GMP level. The precise role of cyclic GMP in platelet activation is not yet known. In order to study the mechanism of action of this drug, we tried to determine the effect of Sin 1 on the different steps described above. We measured Ca2+ fluxes and phospholipase C activation in thrombin (0,5 U/ml) stimulated platelets in the presence of different doses of Sin 1 (10™7-10™3M). Serotonin secretion was inhibited by 30 % with Sin 1 (10™4M-10™5m). A parallel inhibition of phospholipase C was detected by measurement of [32P)-PA level. Platelets loaded with Quin 2 and stimulated by thrombin showed a 70 % inhibition of external Ca2+ influx as soon as a concentration of 10™7M of Sin 1 was added. A study on platelet loaded with [45Ca2+) and Quin 2 confirmed these results. On the contrary, discharge of internal Ca2+ store seemed to be unaffected.In conclusion, the major effect of Sin 1 on platelet phospholipase C pathway is an inhibition of Ca2+ influx through plasma membrane. Some further experiments are necessary to shown whether this inhibition is correlated with cyclic GMP formation (the major effect of Sin 1) and try to establish a relation between this inhibition and that exerted on phospholipase C.Sin 1 was a generous gift of Hoechst.
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