Journal articles: 'Calcium channel drugs'

1

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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9

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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Hedge, Matthew. "Calcium Channel Blocker Toxicology." Journal of Pharmacy Practice 18, no. 3 (June 2005): 169–74. http://dx.doi.org/10.1177/0897190005276749.

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Calcium channel blockers are commonly prescribed antihypertensive medications in the United States and as such are a common presenting ingestion. The pharmacology and mechanism of action of this class of drugs will be discussed. The clinical presentation and therapeutic options will be reviewed.

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12

Collins, William C. J., Michael J. Cullen, and John Feely. "Calcium channel blocker drugs and diabetic control." Clinical Pharmacology and Therapeutics 42, no. 4 (October 1987): 420–23. http://dx.doi.org/10.1038/clpt.1987.172.

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Josefson, D. "Calcium channel blockers inferior to cheaper drugs." BMJ 321, no. 7261 (September 9, 2000): 590. http://dx.doi.org/10.1136/bmj.321.7261.590.

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Schramm, Matthias, and Robertson Towart. "Modulation of calcium channel function by drugs." Life Sciences 37, no. 20 (November 1985): 1843–60. http://dx.doi.org/10.1016/0024-3205(85)90001-3.

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Jayaseelan, Vijayashree Priyadharsini, and Arumugam Paramasivam. "Repurposing calcium channel blockers as antiviral drugs." Journal of Cell Communication and Signaling 14, no. 4 (August 19, 2020): 467–68. http://dx.doi.org/10.1007/s12079-020-00579-y.

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16

Govoni, S., F. Battaini, M. Trabucchi, and R. Paoletti. "CNS effects of calcium channel blocking drugs." International Journal of Developmental Neuroscience 3, no. 4 (1985): 440. http://dx.doi.org/10.1016/0736-5748(85)90135-2.

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Shah, Kajol, Sarah Seeley, Castin Schulz, Jacqueline Fisher, and Shubha Gururaja Rao. "Calcium Channels in the Heart: Disease States and Drugs." Cells 11, no. 6 (March 10, 2022): 943. http://dx.doi.org/10.3390/cells11060943.

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Calcium ions are the major signaling ions in the cells. They regulate muscle contraction, neurotransmitter secretion, cell growth and migration, and the activity of several proteins including enzymes and ion channels and transporters. They participate in various signal transduction pathways, thereby regulating major physiological functions. Calcium ion entry into the cells is regulated by specific calcium channels and transporters. There are mainly six types of calcium channels, of which only two are prominent in the heart. In cardiac tissues, the two types of calcium channels are the L type and the T type. L-type channels are found in all cardiac cells and T-type are expressed in Purkinje cells, pacemaker and atrial cells. Both these types of channels contribute to atrioventricular conduction as well as pacemaker activity. Given the crucial role of calcium channels in the cardiac conduction system, mutations and dysfunctions of these channels are known to cause several diseases and disorders. Drugs targeting calcium channels hence are used in a wide variety of cardiac disorders including but not limited to hypertension, angina, and arrhythmias. This review summarizes the type of cardiac calcium channels, their function, and disorders caused by their mutations and dysfunctions. Finally, this review also focuses on the types of calcium channel blockers and their use in a variety of cardiac disorders.

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Alam, Md Reyaz, Khadga Raj, and Shamsher Singh. "The Roles of Calcium Ions in Parkinson’s Disease: Calcium Channel Inhibitors as a Novel Agents?" Journal of Molecular Pathology 3, no. 4 (October 19, 2022): 243–61. http://dx.doi.org/10.3390/jmp3040021.

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Parkinson’s disease (PD) is a neurodegenerative movement disorder characterized by the loss of dopaminergic neurons, which results in motor impairment. The rationale and objective of the review article is to determine whether CCBs use contributes to a lower risk of developing a first-time diagnosis of PD. Ca2+ homeostasis disruption and mitochondrial dysfunction play a vital role in PD aetiology. In addition, the L-type voltage-gated calcium channel is expressed at high levels amongst nigral neurons, and could play a role in the pathogenesis of PD. In the dopaminergic neurons, Ca2+ entry through plasma membrane Cav1 channels drives a sustained feed-forward stimulation of mitochondrial oxidative phosphorylation. This study investigates the therapeutic potential of R- and T-type Ca2+ channel inhibition in light of new preclinical and clinical data and the feasibility of available Ca2+ channel blockers to cure PD progression. The R-type calcium channel is a type of voltage-dependent calcium channel. Available findings suggest that calcium homeostasis in dopaminergic neurons might be a valuable target for developing new drugs for PD patients. The limitations of our study include reports of observational studies with different follow-up periods. The specific roles of individual drugs and doses were also not mentioned because of nonreporting in the studies.

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Lam, Y. W. Francis. "Calcium Metabolism, Calcium-Channel Blocking Agents, and Hypertension Management." Drug Intelligence & Clinical Pharmacy 22, no. 9 (September 1988): 659–71. http://dx.doi.org/10.1177/106002808802200902.

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Increasing evidence has suggested that a disturbance of cellular calcium metabolism may have a role in initiating and maintaining elevated systemic vascular resistance in essential hypertension. Controversy exists over whether calcium can alleviate or exacerbate the hypertensive process, and diversity of calcium metabolism in hypertensive patients has been proposed. Calcium-channel blocking agents are potent vasodilators capable of correcting the elevated systemic vascular resistance. Clinical studies have shown that these drugs have antihypertensive efficacy comparable to established agents. The elderly, blacks, and patients with low renin activity respond well to calcium-channel blockers. These drugs may also offer potential advantages over established antihypertensive agents in patients with other coexisting diseases. Sustained release formulations have been developed, and initial experience with long-term efficacy and tolerability is encouraging. The calcium-channel blockers may become first-line therapy for treatment of hypertension in selected patients.

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20

Liin, Sara I., Per-Eric Lund, Johan E. Larsson, Johan Brask, Björn Wallner, and Fredrik Elinder. "Biaryl sulfonamide motifs up- or down-regulate ion channel activity by activating voltage sensors." Journal of General Physiology 150, no. 8 (July 12, 2018): 1215–30. http://dx.doi.org/10.1085/jgp.201711942.

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Voltage-gated ion channels are key molecules for the generation of cellular electrical excitability. Many pharmaceutical drugs target these channels by blocking their ion-conducting pore, but in many cases, channel-opening compounds would be more beneficial. Here, to search for new channel-opening compounds, we screen 18,000 compounds with high-throughput patch-clamp technology and find several potassium-channel openers that share a distinct biaryl-sulfonamide motif. Our data suggest that the negatively charged variants of these compounds bind to the top of the voltage-sensor domain, between transmembrane segments 3 and 4, to open the channel. Although we show here that biaryl-sulfonamide compounds open a potassium channel, they have also been reported to block sodium and calcium channels. However, because they inactivate voltage-gated sodium channels by promoting activation of one voltage sensor, we suggest that, despite different effects on the channel gates, the biaryl-sulfonamide motif is a general ion-channel activator motif. Because these compounds block action potential–generating sodium and calcium channels and open an action potential–dampening potassium channel, they should have a high propensity to reduce excitability. This opens up the possibility to build new excitability-reducing pharmaceutical drugs from the biaryl-sulfonamide scaffold.

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Reuter, H., S. Kokubun, and B. Prod'hom. "Properties and modulation of cardiac calcium channels." Journal of Experimental Biology 124, no. 1 (September 1, 1986): 191–201. http://dx.doi.org/10.1242/jeb.124.1.191.

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Voltage-dependent calcium channels are widely distributed in excitable membranes and are involved in the regulation of many cellular functions. These channels can be modulated by neurotransmitters and drugs. There is one particular type of calcium channel in cardiac cells (L-type) whose gating is affected in different ways by beta-adrenoceptor and 1,4-dihydropyridine agonists. We have analysed single calcium channel currents (i) in myocytes from rat hearts in the absence and presence of isoproterenol or 8-bromo-cAMP. We have found that both compounds have similar effects on calcium channel properties. They increase the overall open state probability (po) of individual calcium channels while i remains unaffected. Analysis of the gating kinetics of calcium channels showed: a slight increase in the mean open times of calcium channels, a reduction in time intervals between bursts of channel openings, an increase in burst length and a prominent reduction in failures of calcium channels to open upon depolarization. These kinetic changes caused by isoproterenol and 8-bromo-cAMP can account for the increase in po. Since the macroscopic calcium current, ICa, can be described by ICa = N X po X i, the increase in po accounts for the well-known increase in ICa by beta-adrenergic catecholamines. Cyclic AMP-dependent phosphorylation of calcium channels is a likely metabolic step involved in this modulation. Another class of drug that modulates calcium channel gating is the 1,4-dihydropyridines which can either enhance or reduce ICa, either by prolonging the open state of the channels or by facilitating the inactivated state. Both effects depend strongly on membrane potential and are independent of cyclic AMP-dependent phosphorylation reactions.

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VAGHY, PAL L., KIYOSHI ITAGAKI, KUNIHISA MIWA, EDWARD McKENNA, and ARNOLD SCHWARTZ. "Mechanism of Action of Calcium Channel Modulator Drugs." Annals of the New York Academy of Sciences 522, no. 1 Calcium Antag (March 1988): 176–86. http://dx.doi.org/10.1111/j.1749-6632.1988.tb33353.x.

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23

Luft, Friedrich C. "Calcium-Channel-Blocking Drugs and Renal Sodium Excretion." American Journal of Nephrology 7, no. 1 (1987): 39–43. http://dx.doi.org/10.1159/000167541.

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Kizer, Jorge R., and Stephen E. Kimmel. "Epidemiologic Review of the Calcium Channel Blocker Drugs." Archives of Internal Medicine 161, no. 9 (May 14, 2001): 1145. http://dx.doi.org/10.1001/archinte.161.9.1145.

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25

Zhang, Sui-Po, Jack Kauffman, Susan K. Yagel, and Ellen E. Codd. "High-Throughput Screening for N-Type Calcium Channel Blockers Using a Scintillation Proximity Assay." Journal of Biomolecular Screening 11, no. 6 (June 7, 2006): 672–77. http://dx.doi.org/10.1177/1087057106289210.

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N-type calcium channels located on presynaptic nerve terminals regulate neurotransmitter release, including that from the spinal terminations of primary afferent nociceptors. Accordingly, N-type calcium channel blockers may have clinical utility as analgesic drugs. A selective N-type calcium channel inhibitor, ziconotide (Prialt), is a neuroactive peptide recently marketed as a novel nonopioid treatment for severe chronic pain. To develop a small-molecule N-type calcium channel blocker, the authors developed a 96-well plate high-throughput screening scintillation proximity assay (SPA) for N-type calcium channel blockers using [125I]-labeled ω-conotoxin GVIA as a channel-specific ligand. Assay reagents were handled using Caliper’s Allegro automation system, and bound ligands were detected using a PerkinElmer TopCount. Using this assay, more than 150,000 compounds were screened at 10 μM and approximately 340 compounds were identified as hits, exhibiting at least 40% inhibition of [125I]GVIA binding. This is the 1st demonstration of the use of [125I]-labeled peptides with SPA beads to provide a binding assay for the evaluation of ligand binding to calcium channels. This assay could be a useful tool for drug discovery.

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Shuja, Naveed, Naheed Akhter, Shahnaz Bano Memon, Fareeda Islam, Qamar Zaman Phull, and Mashkoor Ahmed Ansari. "Prospects of Drug Interaction of Metformin with Lifesaving Hypertensive Drugs in Type2 Diabetic Patients. A Clinical Comparative Study." Pakistan Journal of Medical and Health Sciences 16, no. 3 (March 31, 2022): 499–500. http://dx.doi.org/10.53350/pjmhs22163499.

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The aims and objectives of current study was to check and concluded the chances of any drug interaction of metformin with hypertensive treatment with beta- blockers and calcium channel blockers in type 2 diabetic patients. During study diabetic patients with type 2 were treated with metformin and hypertensive drugs i.e. beta- blockers and calcium channel blockers. There is no any drug interaction in both gender has seen (1.00± 00.01, 1.00± 00.01). while Significant change (p<0.05) regarding glucose levels, systolic and diastolic blood pressure were seen in group B and group C as compared to the group A i.e. control group. Keyword: Drug interaction, Metformin, Beta- blockers, Calcium channel blockers

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27

Anikin, G. S. "Pleiotropic features of dihydropyridine calcium channel antagonists." Systemic Hypertension 11, no. 3 (September 15, 2014): 81–83. http://dx.doi.org/10.26442/sg29053.

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It is hard to imagine modern medicine without safe drugs (D). Often, adverse drug reactions (ADR) are the reason for drug with drawal, which is quite effective as a whole. The main dihydropyridine calcium channel antagonists (DCCA) ADR are the edema of shin and tachycardia, causing this drug with drawal. Lercanidipine is aquite new member of this class; it is a highly lipophilic compound, which blocking the influx of calcium ions through L-type calcium channels, by maintaining the high intramembrane concentration. This review provides the data on the efficacy and safety of lercanidipine and its pleiotropic features.

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Coulter, Douglas A. "Antiepileptic Drug Cellular Mechanisms of Action: Where Does Lamotrigine Fit In?" Journal of Child Neurology 12, no. 1_suppl (November 1997): S2—S9. http://dx.doi.org/10.1177/0883073897012001031.

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Current frontline antiepileptic drugs tend to fall into several cellular mechanistic categories, and these categories often correlate with the clinical spectrum of action of the various antiepileptic drugs. Many antiepileptic drugs effective in control of partial and generalized tonic-clonic seizures are use- and voltage-dependent blockers of sodium channels. This mechanism selectively dampens pathologic activation of sodium channels, without interacting with normal sodium channel function. Examples include phenytoin, carbamazepine, valproic acid, and lamotrigine. Many antiepileptic drugs effective in control of generalized absence seizures block low threshold calcium currents. Low threshold calcium channels are present in high densities in thalamic neurons, and these channels trigger regenerative bursts that drive normal and pathologic thalamocortical rhythms, including the spike wave discharges of absence seizures. Examples include ethosuximide, trimethadione, and methsuximide. Several antiepileptic drugs that have varying clinical actions interact with the γ-aminobutyric acid (GABA)ergic system. Diazepam and clonazepam selectively augment function of a subset of GABA A receptors, and these drugs are broad-spectrum antiepileptic drugs. In contrast, barbiturates augment function of all types of GABAA receptors, and are ineffective in control of generalized absence seizures, but effective in control of many other seizure types. Tiagabine and vigabatrin enhance cerebrospinal levels of GABA by interfering with reuptake and degradation of GABA, respectively. These antiepileptic drugs are effective in partial seizures. Lamotrigine is effective against both partial and generalized seizures, including generalized absence seizures. Its sole documented cellular mechanism of action is sodium channel block, a mechanism shared by phenytoin and carbamazepine. These drugs are ineffective against absence seizures. Consequently, unless there are unique aspects to the sodium channel block by lamotrigine, it seems unlikely that this mechanism alone could explain its broad clinical efficacy. Therefore, lamotrigine may have as yet uncharacterized cellular actions, which could combine with its sodium channel blocking actions, to account for its broad clinical efficacy. (J Child Neurol 1997;12(Suppl 1):S2-S9).

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Dolphin, Annette C. "Voltage-gated calcium channels: Their discovery, function and importance as drug targets." Brain and Neuroscience Advances 2 (January 2018): 239821281879480. http://dx.doi.org/10.1177/2398212818794805.

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This review will first describe the importance of Ca2+ entry for function of excitable cells, and the subsequent discovery of voltage-activated calcium conductances in these cells. This finding was rapidly followed by the identification of multiple subtypes of calcium conductance in different tissues. These were initially termed low- and high-voltage activated currents, but were then further subdivided into L-, N-, PQ-, R- and T-type calcium currents on the basis of differing pharmacology, voltage-dependent and kinetic properties, and single channel conductance. Purification of skeletal muscle calcium channels allowed the molecular identification of the pore-forming and auxiliary α2δ, β and ϒ subunits present in these calcium channel complexes. These advances then led to the cloning of the different subunits, which permitted molecular characterisation, to match the cloned channels with physiological function. Studies with knockout and other mutant mice then allowed further investigation of physiological and pathophysiological roles of calcium channels. In terms of pharmacology, cardiovascular L-type channels are targets for the widely used antihypertensive 1,4-dihydropyridines and other calcium channel blockers, N-type channels are a drug target in pain, and α2δ-1 is the therapeutic target of the gabapentinoid drugs, used in neuropathic pain. Recent structural advances have allowed a deeper understanding of Ca2+ permeation through the channel pore and the structure of both the pore-forming and auxiliary subunits. Voltage-gated calcium channels are subject to multiple pathways of modulation by G-protein and second messenger regulation. Furthermore, their trafficking pathways, subcellular localisation and functional specificity are the subjects of active investigation.

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Huguenard, John R. "Block of T-Type Ca²⁺ Channels Is an Important Action of Succinimide Antiabsence Drugs." Epilepsy Currents 2, no. 2 (March 2002): 49–52. http://dx.doi.org/10.1111/j.1535-7597.2002.00019.x.

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The role of calcium channel blockade in the antiepileptic action of ethosuximide is controversial, especially regarding the potency and efficacy of block. However, recent evidence obtained from transgenic animals and heterologous expression systems supports a major role of T-type calcium channels in both the generation of absence seizures and the action of ethosuximide in human absence epilepsy.

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Sowers, James R., George L. Bakris, Henry R. Black, and Thomas D. Giles. "The Cardiometabolic Syndrome and Calcium Channel Blocker Combination Drugs." Journal of the CardioMetabolic Syndrome 2, no. 3 (June 2007): 207–12. http://dx.doi.org/10.1111/j.1559-4564.2007.06656.x.

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Waal-Manning, H. J., and J. M. Paulin. "SODIUM SUPPLEMENTS, BLOOD PRESSURE, AND CALCIUM CHANNEL BLOCKING DRUGS." Lancet 329, no. 8546 (June 1987): 1370. http://dx.doi.org/10.1016/s0140-6736(87)90668-4.

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Ozkul, Yasar. "Influence of calcium channel blocker drugs in neuromuscular transmission." Clinical Neurophysiology 118, no. 9 (September 2007): 2005–8. http://dx.doi.org/10.1016/j.clinph.2007.06.002.

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Rosing, Douglas R., Ulla Idänpään-Heikkilä, Barry J. Maron, Robert O. Bonow, and Stephen E. Epstein. "Use of calcium-channel blocking drugs in hypertrophic cardiomyopathy." American Journal of Cardiology 55, no. 3 (January 1985): B185—B195. http://dx.doi.org/10.1016/0002-9149(85)90630-7.

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Chakraborty, Rajdeep, Honghua Hu, Charbel Darido, Karen Vickery, and Shoba Ranganathan. "ML218 HCl Is More Efficient Than Capsaicin in Inhibiting Bacterial Antigen-Induced Cal 27 Oral Cancer Cell Proliferation." International Journal of Molecular Sciences 22, no. 22 (November 22, 2021): 12559. http://dx.doi.org/10.3390/ijms222212559.

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The bacterial antigen, lipopolysaccharide (LPS) and disruptions in calcium channels are independently known to influence oral cancer progression. Previously, we found that bacterial antigens, LPS and lipoteichoic acid (LTA) act as confounders during the action of capsaicin on Cal 27 oral cancer proliferation. As calcium channel drugs may affect oral cancer cell proliferation, we investigated the effect of ML218 HCl, a T-type voltage-gated calcium channel blocker, on the proliferation of Cal 27 oral cancer cells. We hypothesized that ML218 HCl could effectively reduce LPS-induced oral cancer cell proliferation. LPS and LTA antigens were added to Cal 27 oral cancer cells either prior to and/or concurrently with ML218 HCl treatment, and the efficacy of the treatment was evaluated by measuring Cal 27 proliferation, cell death and apoptosis. ML218 HCl inhibited oral cancer cell proliferation, increased apoptosis and cell death, but their efficacy was significantly reduced in the presence of bacterial antigens. ML218 HCl proved more effective than capsaicin in reducing bacterial antigen-induced Cal 27 oral cancer cell proliferation. Our results also suggest an interplay of proliferation factors during the bacterial antigens and calcium channel drug interaction in Cal 27. Bacterial antigen reduction of drug efficacy should be considered for developing newer pharmacological agents or testing the efficacy of the existing oral cancer chemotherapeutic agents. Finally, voltage gated calcium channel drugs should be considered for future oral cancer research.

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Quirion, Rémi, F. Lafaille, and N. P. V. Nair. "Comparative potencies of calcium channel antagonists and antischizophrenic drugs on central and peripheral calcium channel binding sites." Journal of Pharmacy and Pharmacology 37, no. 6 (June 1985): 437–40. http://dx.doi.org/10.1111/j.2042-7158.1985.tb03033.x.

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Aupetit, Jean-François, Bernard Bui-Xuan, Idriss Kioueh, Joseph Loufoua, Dominique Frassati, and Quadiri Timour. "Opposite change with ischaemia in the antifibrillatory effects of class I and class IV antiarrhythmic drugs resulting from the alteration in ion transmembrane exchanges related to depolarization." Canadian Journal of Physiology and Pharmacology 78, no. 3 (March 1, 2000): 208–16. http://dx.doi.org/10.1139/y99-129.

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It is known that class I antiarrhythmic drugs lose their antifibrillatory activity with severe ischaemia, whereas class IV antiarrhythmic drugs acquire such activity. Tachycardia, which is also a depolarizing factor, has recently been shown to give rise to an alteration of ion transmembrane exchanges which is particularly marked in the case of calcium. This leads one to wonder if the change in antifibrillatory activity of antiarrhythmic drugs caused by ischaemia depends on the same process. The change in antifibrillatory activity was studied in normal conditions ranging to those of severe ischaemia with a class I antiarrhythmic drug, flecainide (1.00 mg·kg-1 plus 0.04 mg·kg-1·min-1), a sodium channel blocker, and a class IV antiarrhythmic drug, verapamil (50 µg·kg-1 plus 2 µg·kg-1·min-1), a calcium channel blocker. The experiments were performed in anaesthetized, open-chest pigs. The resulting blockade of each of these channels was assessed at the end of ischaemic periods of increasing duration (30, 60, 120, 180, 300, and 420 s) by determining the ventricular fibrillation threshold (VFT). VFT was determined by means of trains of diastolic stimuli of 100 ms duration delivered by a subepicardial electrode introduced into the myocardium (heart rate 180 beats per min). Ischaemia was induced by completely occluding the left anterior descending coronary artery. The monophasic action potential was recorded concurrently for the measurement of ventricular conduction time (VCT). The monophasic action potential duration (MAPD) varied with membrane polarization of the fibres. The blockade of sodium channels by flecainide, which normally raises VFT (7.0 ± 0.4 to 13.8 ± 0.8 mA, p < 0.001) and lengthens VCT (28 ± 3 to 44 ± 5 ms, p < 0.001), lost its effects in the course of ischaemia. This resulted in decreased counteraction of the ischaemia-induced fall of VFT and decreased aggravation of the ischaemia-induced lengthening of VCT. The blockade of calcium channels, which normally does not alter VFT (between 7.2 ± 0.6 and 8.4 ± 0.7 mA, n.s.) or VCT (between 30 ± 2 and 34 ± 3 ms, n.s.), slowed the ischaemia-induced fall of VFT. VFT required more time to reach 0 mA, thus delaying the onset of fibrillation. Membrane depolarization itself was opposed as the shortening of MAPD and the lengthening of VCT were also delayed. Consequently there is a progressive decrease in the role played by sodium channels during ischaemia in the rhythmic systolic depolarization of the ventricular fibres. This reduces or suppresses the ability of sodium channel blockers to act on excitability or conduction, and increases the role of calcium channel blockers in attenuating ischaemia-induced disorders.Key words: pigs, ion transmembrane exchanges, myocardial ischaemia, sodium channel, calcium channel.

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38

Baeyens, José M. "Interactions between Calcium Channel Blockers and Non-Cardiovascular Drugs: Interactions with Anticancer Drugs." Pharmacology & Toxicology 63, no. 1 (July 1988): 1–7. http://dx.doi.org/10.1111/j.1600-0773.1988.tb00899.x.

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Joshi, Sanjeev, and Sucheta Bansal. "A Rare Case Report of Amlodipine-Induced Gingival Enlargement and Review of Its Pathogenesis." Case Reports in Dentistry 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/138248.

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Gingival enlargement is a common clinical feature of gingival and periodontal diseases. It is an unwanted side effect of certain systemic drugs given for nondental treatment. It is being reported with three main groups of drugs like calcium channel blockers (CCBs), immunosuppressants, and anticonvulsants. Among calcium channel blockers, nifedipine causes gingival hyperplasia in about 10% of patients, whereas the incidence of amlodipine-, a third generation calcium channel blocker, induced gingival hyperplasia is very limited. There are very few reports of amlodipine-induced gingival enlargement at a dose of 5 mg. We report a case of amlodipine-induced gingival enlargement in a 45-year-old hypertensive patient taking amlodipine at a dose of 5 mg.

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40

Payandeh, Jian. "Crystallographic studies of voltage-gated sodium and calcium channels." Acta Crystallographica Section A Foundations and Advances 70, a1 (August 5, 2014): C1488. http://dx.doi.org/10.1107/s2053273314085118.

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Voltage-gated ion channels (VGICs) mediate electrical signaling within the nervous system and regulate a wide range of physiological processes. Voltage-gated sodium (Nav) channels are responsible for initiating action potentials and their rapid activation, sodium selectivity, and drug sensitivity are unique among VGICs. Nav channels are the molecular targets of drugs used in local anaesthesia and in the treatment of genetic and sporadic Nav channelopathies including inherited epilepsy, migraine, periodic paralysis, cardiac arrhythmia, and chronic pain syndromes. Recent crystal structures of a Nav channel from the bacterium Arcobacter butzleri (NavAb) have revealed surprising insights into the structural basis for voltage-dependent activation, sodium selectivity, drug block, and slow inactivation (1,2). The available structures of NavAb will be described alongside complementary functional and molecular dynamic studies. Distinct from Nav channels, the closely related voltage-gated calcium (Cav) channels initiate processes such as synaptic transmission, muscle contraction, and hormone secretion in response to membrane depolarization. Cav channels catalyze the rapid and highly selective influx of calcium ions into cells despite a 70-fold higher extracellular concentration of sodium. By grafting a Cav channel selectivity filter onto NavAb, crystallographic and functional analyses of the resulting CavAb channel will be described that have revealed a multi-ion selectivity filter which establishes a structural framework for understanding the mechanisms of ion selectivity and conductance in vertebrate Cav channels (3).

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41

Bhardwaj, Rajesh, Sonja Lindinger, Arthur Neuberger, Kirill D. Nadezhdin, Appu K. Singh, Micael R. Cunha, Isabella Derler, et al. "Inactivation-mimicking block of the epithelial calcium channel TRPV6." Science Advances 6, no. 48 (November 2020): eabe1508. http://dx.doi.org/10.1126/sciadv.abe1508.

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Epithelial calcium channel TRPV6 plays vital roles in calcium homeostasis, and its dysregulation is implicated in multifactorial diseases, including cancers. Here, we study the molecular mechanism of selective nanomolar-affinity TRPV6 inhibition by (4-phenylcyclohexyl)piperazine derivatives (PCHPDs). We use x-ray crystallography and cryo–electron microscopy to solve the inhibitor-bound structures of TRPV6 and identify two types of inhibitor binding sites in the transmembrane region: (i) modulatory sites between the S1-S4 and pore domains normally occupied by lipids and (ii) the main site in the ion channel pore. Our structural data combined with mutagenesis, functional and computational approaches suggest that PCHPDs plug the open pore of TRPV6 and convert the channel into a nonconducting state, mimicking the action of calmodulin, which causes inactivation of TRPV6 channels under physiological conditions. This mechanism of inhibition explains the high selectivity and potency of PCHPDs and opens up unexplored avenues for the design of future-generation biomimetic drugs.

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Ardura, Juan A., Luis Álvarez-Carrión, Irene Gutiérrez-Rojas, and Verónica Alonso. "Role of Calcium Signaling in Prostate Cancer Progression: Effects on Cancer Hallmarks and Bone Metastatic Mechanisms." Cancers 12, no. 5 (April 25, 2020): 1071. http://dx.doi.org/10.3390/cancers12051071.

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Advanced prostate cancers that progress to tumor metastases are often considered incurable or difficult to treat. The etiology of prostate cancers is multi-factorial. Among other factors, de-regulation of calcium signals in prostate tumor cells mediates several pathological dysfunctions associated with tumor progression. Calcium plays a relevant role on tumor cell death, proliferation, motility-invasion and tumor metastasis. Calcium controls molecular factors and signaling pathways involved in the development of prostate cancer and its progression. Such factors and pathways include calcium channels and calcium-binding proteins. Nevertheless, the involvement of calcium signaling on prostate cancer predisposition for bone tropism has been relatively unexplored. In this regard, a diversity of mechanisms triggers transient accumulation of intracellular calcium in prostate cancer cells, potentially favoring bone metastases development. New therapies for the treatment of prostate cancer include compounds characterized by potent and specific actions that target calcium channels/transporters or pumps. These novel drugs for prostate cancer treatment encompass calcium-ATPase inhibitors, voltage-gated calcium channel inhibitors, transient receptor potential (TRP) channel regulators or Orai inhibitors. This review details the latest results that have evaluated the relationship between calcium signaling and progression of prostate cancer, as well as potential therapies aiming to modulate calcium signaling in prostate tumor progression.

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43

Tedford, H. William, Alexandra E. Kisilevsky, Jean B. Peloquin, and Gerald W. Zamponi. "Scanning Mutagenesis Reveals a Role for Serine 189 of the Heterotrimeric G-Protein Beta 1 Subunit in the Inhibition of N-Type Calcium Channels." Journal of Neurophysiology 96, no. 1 (July 2006): 465–70. http://dx.doi.org/10.1152/jn.00216.2006.

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Direct interactions between the presynaptic N-type calcium channel and the β subunit of the heterotrimeric G-protein complex cause voltage-dependent inhibition of N-type channel activity, crucially influencing neurotransmitter release and contributing to analgesia caused by opioid drugs. Previous work using chimeras of the G-protein β subtypes Gβ1 and Gβ5 identified two 20–amino acid stretches of structurally contiguous residues on the Gβ1 subunit as critical for inhibition of the N-type channel. To identify key modulation determinants within these two structural regions, we performed scanning mutagenesis in which individual residues of the Gβ1 subunit were replaced by corresponding Gβ5 residues. Our results show that Gβ1 residue Ser189 is critical for N-type calcium channel modulation, whereas none of the other Gβ1 mutations caused statistically significant effects on the ability of Gβ1 to inhibit N-type channels. Structural modeling shows residue 189 is surface exposed, consistent with the idea that it may form a direct contact with the N-type calcium channel α1 subunit during binding interactions.

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44

Gunawan, Gunawan, Suhardjo Sitam, and Lusi Epsilawati. "Densitas tulang mandibula pengguna obat anti hipertensi calcium channel blocker (CCB) melalui radiograf panoramik." Jurnal Radiologi Dentomaksilofasial Indonesia 4, no. 2 (August 31, 2020): 1. http://dx.doi.org/10.32793/jrdi.v4i2.527.

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Objectives: The purpose of this research was to describe radiographic density of mandibular bone in calcium channel blocker anti-hypertensive drug users. Bone density in the mandible is assessed from the trabecular. Panoramic radiograph is a routine examination that is often done in dentistry that can be used to assess changes in quality in the form of changes in bone density in users of anti-hypertensive calcium channel blockers Material and Methods: This research is a descriptive study of 21 panoramic radiographs of calcium channel blocker anti-hypertensive drug users aged 40-75 years. Panoramic radiograph archive density checks in the distal region of the foramen mentale and the mandibular angular region using software image j, with the final result was the percentage between bone and marrow. Results: This research showed the average radiographic density in male using calcium channel blocker antihypertensive drugs was 18.81% and the average radiographic density in female was 20.92%. Conclusion: Based on the results of the study found that the average radiographic density of female patients taking antihypertensive drugs calcium channel blockers was higher than male.

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Tikhonov, Denis B., and Boris S. Zhorov. "Computational Analysis of the Crystal and Cryo-EM Structures of P-Loop Channels with Drugs." International Journal of Molecular Sciences 22, no. 15 (July 29, 2021): 8143. http://dx.doi.org/10.3390/ijms22158143.

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The superfamily of P-loop channels includes various potassium channels, voltage-gated sodium and calcium channels, transient receptor potential channels, and ionotropic glutamate receptors. Despite huge structural and functional diversity of the channels, their pore-forming domain has a conserved folding. In the past two decades, scores of atomic-scale structures of P-loop channels with medically important drugs in the inner pore have been published. High structural diversity of these complexes complicates the comparative analysis of these structures. Here we 3D-aligned structures of drug-bound P-loop channels, compared their geometric characteristics, and analyzed the energetics of ligand-channel interactions. In the superimposed structures drugs occupy most of the sterically available space in the inner pore and subunit/repeat interfaces. Cationic groups of some drugs occupy vacant binding sites of permeant ions in the inner pore and selectivity-filter region. Various electroneutral drugs, lipids, and detergent molecules are seen in the interfaces between subunits/repeats. In many structures the drugs strongly interact with lipid and detergent molecules, but physiological relevance of such interactions is unclear. Some eukaryotic sodium and calcium channels have state-dependent or drug-induced π-bulges in the inner helices, which would be difficult to predict. The drug-induced π-bulges may represent a novel mechanism of gating modulation.

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Katz, Arnold M., W. David Hager, Frank C. Messineo, and Achilles J. Pappano. "Cellular actions and pharmacology of the calcium channel blocking drugs." American Journal of Medicine 79, no. 4 (October 1985): 2–10. http://dx.doi.org/10.1016/0002-9343(85)90494-2.

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Tuffin, D. P., and P. J. Wade. "Calcium channel blocking drugs: A structural lead for PAF antagonists?" Prostaglandins 30, no. 4 (October 1985): 702. http://dx.doi.org/10.1016/0090-6980(85)90046-2.

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48

Cho, Cornelia. "Therapeutic Uses of Calcium Channel-Blocking Drugs in the Young." Archives of Pediatrics & Adolescent Medicine 140, no. 4 (April 1, 1986): 360. http://dx.doi.org/10.1001/archpedi.1986.02140180094034.

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49

Chazova, I. E., and Yu V. Zhernakova. "Calcium channel blockers: more than 50 years on guard of health." Systemic Hypertension 12, no. 2 (June 15, 2015): 49–56. http://dx.doi.org/10.26442/sg29074.

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The class of drugs - calcium antagonists (CA), or calcium channel blockers (CCBs) is combined a quite heterogeneous drugs group possessing common vasodilatatory characteristics by disruption of the movement of calcium through the vascular smooth muscle cells and with different degree of impact on myocardium, the sinus node function, atrioventricular conduction, tonus of peripheral vessels and coronary blood flow. The existence of this class of drugs has become one of the great achievements in the field of pharmacology, at the end of the 20th century. Third Generation CCBs takes the special place in hypertensiology because of high bioavailability and tissue selectivity. Modern long-acting CA are widely used in case of arterial hypertension (AH), they can be used especially in patients with diabetes mellitus, peripheral artery disease, chronic obstructive pulmonary disease and bronchial asthma, ischemic heart disease and in elderly patients with systolic AH. These drugs show not only antihypertensive effect and organoprotective characteristics, but also can improve the prognosis in patients with high and very high cardiovascular risk.

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Naumovic, Nada, Petar Slankamenac, Danka Filipovic, Vesna Ivetic, Snezana Tomasevic-Todorovic, and Ksenija Boskovic. "Effects of calcium antagonists on brain ischemia." Medical review 64, no. 5-6 (2011): 257–61. http://dx.doi.org/10.2298/mpns1106257n.

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Introduction. Stroke is the second leading cause of death in the world and the leading cause of serious, long term disability in adults; about half of those who survive become dependent on others in performing personal activities of daily living. Ischemia disturbs calcium cellular homeostasis, whereas calcium channel blockers re-establish it. This study was aimed at assessing benefits of calcium channel blockers on the outcome of rehabilitation of the patients afflicted by ischemic stroke. Material and Methods. The functional independence was measured by the Barthel index in 90 patients subjected to rehabilitative therapeutic treatment. The functional recovery of patients treated with calcium channel blockers and with other drugs (control) was compared and tested. Results. The analysis of variance (ANOVA) for the 0.5 confidence interval showed that the increases of the Barthel index values were significantly higher in the patients treated with calcium antagonists (p<0.5). Discussion. According to the literature, such an outcome is the result of improved brain blood f low auto-regulation, increased brain perfusion as well as of neuroprotective, antioxidative, platelet antiaggregatory effects of investigated drugs. Conclusion. The calcium channel blockers improved the outcome of rehabilitative therapeutic treatment significantly in the patients afflicted by ischemic stroke.

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Journal articles on the topic 'Calcium channel drugs'

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