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Relevant bibliographies by topics / Ca++-channels blocker

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Academic literature on the topic 'Ca++-channels blocker'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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Journal articles on the topic "Ca++-channels blocker"

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Lei, Jianzhen, Xiaoxin Liu, Miaomiao Song, et al. "Aberrant Exon 8/8a Splicing by Downregulated PTBP (Polypyrimidine Tract-Binding Protein) 1 Increases Ca V 1.2 Dihydropyridine Resistance to Attenuate Vasodilation." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 10 (2020): 2440–53. http://dx.doi.org/10.1161/atvbaha.120.315010.

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Objective: Calcium channel blockers, such as dihydropyridines, are commonly used to inhibit enhanced activity of vascular Ca V 1.2 channels in hypertension. However, patients who are insensitive to such treatments develop calcium channel blocker-resistant hypertension. The function of Ca V 1.2 channel is diversified by alternative splicing, and the splicing factor PTBP (polypyrimidine tract-binding protein) 1 influences the utilization of mutually exclusive exon 8/8a of the Ca V 1.2 channel during neuronal development. Nevertheless, whether and how PTBP1 makes a role in the calcium channel blo

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Nagayama, Takahiro, Kimiya Masada, Makoto Yoshida, et al. "Role of K+ channels in adrenal catecholamine secretion in anesthetized dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 4 (1998): R1125—R1130. http://dx.doi.org/10.1152/ajpregu.1998.274.4.r1125.

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We examined the role of K+ channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K+ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K+ channel (KA type) blocker mast cell degranulating (MCD) peptide infusion (10–100 ng/min) enhanced increases in CA output induced by SNS (1–3 Hz), but it did not affect increases in CA output induced by ACh (0.75–3 μg), DMPP (0.

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Neyton, J., and M. Pelleschi. "Multi-ion occupancy alters gating in high-conductance, Ca(2+)-activated K+ channels." Journal of General Physiology 97, no. 4 (1991): 641–65. http://dx.doi.org/10.1085/jgp.97.4.641.

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In this study, single-channel recordings of high-conductance Ca(2+)-activated K+ channels from rat skeletal muscle inserted into planar lipid bilayer were used to analyze the effects of two ionic blockers, Ba2+ and Na+, on the channel's gating reactions. The gating equilibrium of the Ba(2+)-blocked channel was investigated through the kinetics of the discrete blockade induced by Ba2+ ions. Gating properties of Na(+)-blocked channels could be directly characterized due to the very high rates of Na+ blocking/unblocking reactions. While in the presence of K+ (5 mM) in the external solution Ba2+ i

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Wilkinson, M. F., and S. Barnes. "The dihydropyridine-sensitive calcium channel subtype in cone photoreceptors." Journal of General Physiology 107, no. 5 (1996): 621–30. http://dx.doi.org/10.1085/jgp.107.5.621.

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High-voltage activated Ca channels in tiger salamander cone photoreceptors were studied with nystatin-permeabilized patch recordings in 3 mM Ca2+ and 10 mM Ba2+. The majority of Ca channel current was dihydropyridine sensitive, suggesting a preponderance of L-type Ca channels. However, voltage-dependent, incomplete block (maximum 60%) by nifedipine (0.1-100 microM) was evident in recordings of cones in tissue slice. In isolated cones, where the block was more potent, nifedipine (0.1-10 microM) or nisoldipine (0.5-5 microM) still failed to eliminate completely the Ca channel current. Nisoldipin

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Blundon, J. A., S. N. Wright, M. S. Brodwick, and G. D. Bittner. "Presynaptic calcium-activated potassium channels and calcium channels at a crayfish neuromuscular junction." Journal of Neurophysiology 73, no. 1 (1995): 178–89. http://dx.doi.org/10.1152/jn.1995.73.1.178.

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1. We used a two-microelectrode current clamp to investigate various characteristics of the Ca(2+)-activated K+ conductance [gK(Ca)] and Ca2+ conductance (gCa), and transmitter release in presynaptic terminals of excitatory neuromuscular junctions in the crayfish walking leg. 2. Voltage-activated Na+ conductances (gNa) and K+ conductances [gK(v)] were blocked with tetrodotoxin and 3,4-diaminopyridine, respectively. Under these conditions, presynaptic depolarization produced by a first (conditioning) pulse admitted Ca2+ into the presynaptic terminals and activated gK(Ca), which modulated the am

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Kamishima, T., M. T. Nelson, and J. B. Patlak. "Carbachol modulates voltage sensitivity of calcium channels in bronchial smooth muscle of rats." American Journal of Physiology-Cell Physiology 263, no. 1 (1992): C69—C77. http://dx.doi.org/10.1152/ajpcell.1992.263.1.c69.

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The role of voltage-dependent Ca channels in carbachol (CCh)-induced contraction of rat bronchus was investigated. Membrane depolarization and BAY K 8644, a Ca channel opener, significantly enhanced CCh-induced contractions. Nisoldipine, an organic Ca channel blocker, significantly inhibited the contractions. Cadmium, an inorganic Ca channel blocker, completely inhibited maintained contractions caused by CCh. These results suggested that the voltage-dependent Ca channels play an important role in sustained cholinergic contractions. This hypothesis was tested further by investigating the proper

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Smith, Forrest L., Richard W. Davis, and Richard Carter. "Influence of Voltage-sensitive Ca++Channel Drugs on Bupivacaine Infiltration Anesthesia in Mice." Anesthesiology 95, no. 5 (2001): 1189–97. http://dx.doi.org/10.1097/00000542-200111000-00024.

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Background Local anesthesia has been traditionally associated with blockade of voltage-sensitive sodium (Na(+)) channels. Yet in vitro evidence indicates that local anesthetic mechanisms are more complex than previously understood. For example, local anesthetics bind and allosterically modify 1,4-dihydropyridine-sensitive Ca(++) channels and can reduce Ca(++) influx in tissues. The current study examines the influence of voltage-sensitive Ca(++) channels in bupivacaine infiltration anesthesia. Methods Baseline tail-flick latencies to radiant heat nociception were obtained before subcutaneous i

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McCann, J. D., and M. J. Welsh. "Neuroleptics antagonize a calcium-activated potassium channel in airway smooth muscle." Journal of General Physiology 89, no. 2 (1987): 339–52. http://dx.doi.org/10.1085/jgp.89.2.339.

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We examined the effect of neuroleptics on Ca-activated K channels from dog airway smooth muscle cells. Because these agents inhibit a variety of other Ca-mediated processes, it seemed possible that they might also inhibit Ca-activated K channels. In excised, inside-out patches, several neuroleptics potently and reversibly inhibited the K channel from the internal but not the external surface of the patch. Measurements of the effect on open probability and open- and closed-state durations support a simple kinetic model in which neuroleptics bind to and block the open channel. Inhibition by neur

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Moore, Christopher L., Samantha J. McClenahan, Hillary M. Hanvey, et al. "Beta1-Adrenergic Receptor-Mediated Dilation of Rat Cerebral Artery Requires Shaker-Type KV1 Channels on PSD95 Scaffold." Journal of Cerebral Blood Flow & Metabolism 35, no. 9 (2015): 1537–46. http://dx.doi.org/10.1038/jcbfm.2015.91.

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Postsynaptic density-95 (PSD95) is a scaffolding protein in cerebral vascular smooth muscle cells (cVSMCs), which binds to Shaker-type K+ (KV1) channels and facilitates channel opening through phosphorylation by protein kinase A. β1-Adrenergic receptors (β1ARs) also have a binding motif for PSD95. Functional association of β1AR with KV1 channels through PSD95 may represent a novel vasodilator complex in cerebral arteries (CA). We explored whether a β1AR-PSD95-KV1 complex is a determinant of rat CA dilation. RT-PCR and western blots revealed expression of β1AR in CA. Isoproterenol induced a con

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Meguro, Toshinari, Christoph P. R. Klett, Betty Chen, Andrew D. Parent, and John H. Zhang. "Role of calcium channels in oxyhemoglobin-induced apoptosis in endothelial cells." Journal of Neurosurgery 93, no. 4 (2000): 640–46. http://dx.doi.org/10.3171/jns.2000.93.4.0640.

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Object. Oxyhemoglobin (OxyHb) released from hemolysed erythrocytes has been considered to be responsible for cerebral vasospasm after subarachnoid hemorrhage. The authors previously reported that OxyHb produced apoptosis in cultured vascular endothelial cells. The change in intracellular Ca++ homeostasis was expected to be one of the possible mechanisms of the cytotoxic effects of OxyHb. This study was undertaken to investigate the protective effects of Ca++-channel blockers on OxyHb-induced apoptosis.Methods. Cultured bovine coronary artery and brain microvascular endothelial cells (passages

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Dissertations / Theses on the topic "Ca++-channels blocker"

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Iwamuro, Yasushi. "Activation of three types of voltage-independent Ca^{2+} channel in A7r5 cells by endothelin-1 as revealed by a novel Ca^{2+} channel blocker LOE908." Kyoto University, 1999. http://hdl.handle.net/2433/181728.

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Ninomiya, Tomonori. "Verapamil, a Ca[2+] entry blocker, targets the pore-forming subunit of cardiac type K[ATP] channel (Kir6.2)." Kyoto University, 2004. http://hdl.handle.net/2433/147501.

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Book chapters on the topic "Ca++-channels blocker"

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Lenzi, G. L., H. Baasch, and R. Bruno. "Neuronal Protection: Is There a Role for Gangliosides or Ca+2-Channel Blockers?" In Thrombolytic Therapy in Acute Ischemic Stroke II. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78061-5_37.

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Hanck, D. A., M. F. Sheets, and H. A. Fozzard. "State-Dependent Block of Cardiac Na Currents by Ca Channel Antagonists." In Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74317-7_13.

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Rahman, Taufiq, and M. O. Faruk Khan. "Ca⁺² Channel Blockers." In Medicinal Chemistry for Pharmacy Students. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815179729124030005.

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This chapter is a comprehensive account of the medicinal chemistry of antihypertensive drugs, Ca2+-channel blockers (CCBs). It provides the mechanism of drug action and detailed structure-activity relationships (SAR) of the CCBs to give the knowledge base for pharmacists. After studying this chapter, students will be able to: • Comprehend the historical background of the CCBs. • Classify different types of voltage-gated Ca2+ channels (VGCCs) and their clinical significance. • Explain CCBs and their clinical significance. • Describe the mechanisms of action of CCBs at the molecular level includ

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"External Ca Ions Block Na Conducting Ca Channel by Promoting Open to Closed Transitions." In Receptors and lon Channels. De Gruyter, 1987. http://dx.doi.org/10.1515/9783112328446-017.

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Endou, Kyoko, Yoshihiro Nara, Hareaki Yamamoto, and Toshiro Sato. "Antiarrhythmic effects of Ca channel blockers on canine Purkinje fibers." In Electrocardiology ’87. De Gruyter, 1988. http://dx.doi.org/10.1515/9783112484289-020.

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Endou, Kyoko, Yoshihiro Nara, Hareaki Yamamoto, and Toshiro Sato. "Antiarrhythmic effects of Ca channel blockers on canine Purkinje fibers." In Electrocardiology ’87. De Gruyter, 1988. http://dx.doi.org/10.1515/9783112542385-020.

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Beswick, P. "Progress in the Discovery of Ca Channel Blockers for the Treatment of Pain." In Comprehensive Medicinal Chemistry III. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-409547-2.12438-2.

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Hillenbrand, Ian, Michael L. Williams, Michael J. Jercinovic, Matthew T. Heizler, and Daniel J. Tjapkes. "Petrochronologic constraints on Paleozoic tectonics in southern New England." In Laurentia: Turning Points in the Evolution of a Continent. Geological Society of America, 2022. http://dx.doi.org/10.1130/2022.1220(25).

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ABSTRACT The Appalachian Mountains were formed through multiple phases of Paleozoic orogenesis associated with terrane accretion. The timing, tempo, and significance of each event in New England are obscured by overprinting, the limits of geochronologic tools, and differences between lithotectonic domains. We present new monazite and xenotime geochronology, 40Ar/39Ar thermochronology, and major- and trace-element thermobarometry from major tectonic domains in southern New England and across multiple structural levels. These data show contrasting pressure-temperature-time (P-T-t) paths across t

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Xie, Yuling, Philip L. Verplanck, Zengqian Hou, and Richen Zhong. "Chapter 12 Rare Earth Element Deposits in China: A Review and New Understandings." In Mineral Deposits of China. Society of Economic Geologists, 2019. http://dx.doi.org/10.5382/sp.22.12.

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Abstract China has been the world’s leading rare earth element (REE) and yttrium producer for more than 20 years and hosts a variety of deposit types. Carbonatite-related REE deposits are the most significant REE deposit type, with REY (REE and yttrium)-bearing clay deposits, or ion adsorption-type deposits, being the primary source of the world’s heavy REEs. Other REY resources in China include those hosted in placers, alkaline granites, pegmatites, and hydrothermal veins, as well as in additional deposit types in which REEs may be recovered as by-product commodities. Carbonatite-related REE

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Zhao, Xinfu, Wei Terry Chen, Xiaochun Li, and Meifu Zhou. "Chapter 13 Iron Oxide Copper-Gold Deposits in China: A Review and Perspectives on Ore Genesis." In Mineral Deposits of China. Society of Economic Geologists, 2019. http://dx.doi.org/10.5382/sp.22.13.

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Abstract Iron oxide copper-gold (IOCG) deposits are hydrothermal deposits characterized by abundant low-Ti Fe oxides, economic Cu-Au grades, structurally controlled orebodies, widespread presulfide alkaline alteration, and commonly significant volumes of breccia. They may also have elevated U, Co, Ag, and rare earth elements (REEs), and may have no clear spatial association with igneous intrusions. The IOCG sensu stricto deposits are rare in China, but the Proterozoic Fe-Cu-(Au-REE) deposits in the Kangdian region, southwestern China, have been confirmed to be of this type. Other related hydro

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Conference papers on the topic "Ca++-channels blocker"

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Anreddy, Nagaraju. "Abstract 1967: A-803467, a sodium channel blocker, reverses ABCG2-mediated MDR." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1967.

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Kawada, Toru, Hiromi Yamamoto, Shuji Shimizu, Michael J. Turner, and Masaru Sugimachi. "Effects of L-type Ca²⁺ channel blocker nifedipine on dynamic arterial blood pressure control." 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.2013.6610373.

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Bevan, Jane, and S. Heptinstall. "BOW CAN WE INHIBIT 5HT-INDUCED PLATELET AGGREGATION AND WHY SHOULD WE BOTHER?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643853.

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Platelets are induced to aggregate when 5-hydraxytryptamine (5HT) is added to citrated whole blood and the extent of aggregation can be measured using a Whole Blood Platelet Counter. We have used this method to study a) 5HT-induced platelet aggregation in normal human blood and the effects of 14 5HT receptor antagonists and 2 Ca++-channel blockers, and b) aggregation in blood from patients with peripheral vascular disease (PVD). Previous studies of platelet aggregation in platelet-rich plasma have indicated an increased platelet sensitivity to 5HT in PVD, and a multicentre study of ketanserin

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Chesney, C. M., and D. D. Pifer. "EFFECT OF Ca2+ and Mg2+ ON PLATELET ACTIVATING FACTOR (PAF) INDUCED AGGREGATION AND SPECIFIC BINDING TO HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642879.

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Gel filtered human platelets (GFP) collected in Tyrode's buffer containing 0.5 mM Ca+2, ImM Mg+2, and 0.35% albumin exhibit high affinity binding of 3H-PAF with a Kd of 0.109 α 0.029 nM (mean α SD; n=13) and 267 α 70 sites per platelet. When fibrinogen (1.67 mg/ml final concentration) is added to these GFP preparations biphasic aggregation is observed with PAF (4 nM). Normal aggregation is also observed with other platelet agonists including ADP, epinephrine, collagen, arachidonic acid, A23187 and thrombin. If GFP is prepared without added Ca+2 or Mg+2 in the presence of 3mM EDTA, platelets do

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Almazan, E. M. P., O. Ellaicy, D. J. Carter, K. Kaleka, and M. A. Faruqi. "Another Case of the Blues, Methylene Blue as Adjunctive Therapy in Calcium-channel Blocker Induced Vasoplegia." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5655.

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Zhao, R., B. Lopez, A. Schwingshackl, and S. Goldstein. "Designed Peptide Blocker of Voltage-Gated Proton Channel (Hv1) Protects Against Lipopolysaccharide (LPS)-Induced Acute Lung Injury." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2520.

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Reports on the topic "Ca++-channels blocker"

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Yibchok-anun, Sirinthorn, Wijit Banlunara, and Sirichai Adisakwattana. Antidiabetic effects, mechanisms of of p-methoxy-trans-cinnamic acid. Faculty of Veterinary Science, Chulalongkorn University, 2008. https://doi.org/10.58837/chula.res.2008.81.

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p-Methoxycinnamic acid (p-MCA) is a cinnamic acid derivative that shows various pharmacologic actions such as neuroprotective and hepatoprotective activities. To examine the insulinotropic activity of p-MCA, the perfused rat pancreas and a pancreatic β-cell line, INS-1 were used in the studies. P-MCA increased insulin secretion from the perfused rat pancreas and INS-1 cells in a concentration-dependent manner. In addition, p-MCA increased intracellular Ca²⁺ concentration ([Ca²⁺]i) in INS-1 cells. The p-MCA-induced insulin secretion and rise in [Ca²⁺]i were markedly inhibited in the absence of

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