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Journal articles on the topic 'Calcium channel drugs'

Author: Grafiati

Published: 10 December 2022

Last updated: 31 July 2025

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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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2

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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3

Triggle, David J. "Calcium, calcium channels, and calcium channel antagonists." Canadian Journal of Physiology and Pharmacology 68, no. 11 (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 th

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4

MILLER-HANCE, WANDA C. "Calcium Channel-Blocking Drugs." Archives of Pediatrics & Adolescent Medicine 140, no. 12 (1986): 1216. http://dx.doi.org/10.1001/archpedi.1986.02140260018012.

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5

Chen, Xinzhe. "Research progress on calcium-activated potassium ion channels." Theoretical and Natural Science 62, no. 1 (2024): 160–65. http://dx.doi.org/10.54254/2753-8818/62/20241522.

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Abstract. Potassium ion channels are diverse and widely distributed, playing a key role in a variety of physiological and pathological processes. According to the size of the conductance, they can be divided into large conductive calcium activated potassium channel (BK channel), medium conductive calcium activated potassium channel (IK channel) and small conductive calcium activated potassium channel (SK channel). In recent years, remarkable progress has been made in studying these three ion channels, and a series of therapeutic drugs have emerged. According to the single channel conductance,

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6

Schoenfeld, N., J. Aelion, Y. Beigel, O. Epstein, and A. Atsmon. "The porphyrogenic effects of calcium channel blocking drugs." Clinical Science 69, no. 5 (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 concentra

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7

Muralinath, E., Devi Pooja, Chbukdhara Prasanta, et al. "Drugs Acting on Arrhythmics." Journal of Advanced Research and Reviews in Virology & Microbiology 1, no. 1 (2024): 10–12. https://doi.org/10.5281/zenodo.10716057.

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<em>Antiarrhythmic drugs play a key role regarding abnormal heart rhythms. Anti-arrhythmic drugs are divided into different classes dependent on their primary mechanism of action. These drugs are regarded as into four main categories such as class I (sodium channel blockers), class II(beta _ blockers), class III (potassium channel blockers) and class IV (calcium channel blockers). Class I anti arrhythmics specifically act on sodium channels, which play a role in the initiation and conduction of action potentials particularly in Cardiac cells. Class II anti arrhythmics act by decreasing the eff

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8

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

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9

White, Pamela. "Calcium Channel Blockers." AACN Advanced Critical Care 3, no. 2 (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

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10

Qiu, Yong, Chiyu Ma, Nan Jiang, et al. "A Silicon-Based Field-Effect Biosensor for Drug-Induced Cardiac Extracellular Calcium Ion Change Detection." Biosensors 14, no. 1 (2023): 16. http://dx.doi.org/10.3390/bios14010016.

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Calcium ions participate in the regulation of almost all biological functions of the body, especially in cardiac excitation–contraction coupling, acting as vital signaling through ion channels. Various cardiovascular drugs exert their effects via affecting the ion channels on the cell membrane. The current strategies for calcium ion monitoring are mainly based on fluorescent probes, which are commonly used for intracellular calcium ion detection (calcium imaging) and cannot achieve long-term monitoring. In this work, an all-solid-state silicone–rubber ion-sensitive membrane was fabricated on l

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11

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 (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 t

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12

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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13

Nappi, Jean M., Jacqueline S. Marinac, and Patricia Bartlomé. "Calcium Channel Blockers." Journal of Pharmacy Practice 3, no. 5 (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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14

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 (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 a

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15

Hedge, Matthew. "Calcium Channel Blocker Toxicology." Journal of Pharmacy Practice 18, no. 3 (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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16

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 (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 t

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17

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 (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 throu

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18

Reuter, H., S. Kokubun, and B. Prod'hom. "Properties and modulation of cardiac calcium channels." Journal of Experimental Biology 124, no. 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 pro

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19

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

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20

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

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21

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

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22

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

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23

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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24

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 (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-ty

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25

Lam, Y. W. Francis. "Calcium Metabolism, Calcium-Channel Blocking Agents, and Hypertension Management." Drug Intelligence & Clinical Pharmacy 22, no. 9 (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.

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26

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

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27

Coulter, Douglas A. "Antiepileptic Drug Cellular Mechanisms of Action: Where Does Lamotrigine Fit In?" Journal of Child Neurology 12, no. 1_suppl (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 effe

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28

Allert, J. Alan, and H. Richard Adams. "New perspectives in cardiovascular medicine: The calcium channel blocking drugs." Journal of the American Veterinary Medical Association 190, no. 5 (1987): 573–78. https://doi.org/10.2460/javma.1987.190.05.573.

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Summary Calcium channel blocking drugs reduce the influx of calcium (Ca++) through cell membrane passageways in excitable tissues. This unique pharmacodynamic action represents an important new addition to cardiovascular therapeutics. Clinically available members of this diverse group of compounds are verapamil, nifedipine, and diltiazem. Beneficial responses to these drugs can be explained by vasodilatation and resulting hemodynamic improvement in tissue perfusion-oxygen demand relationships, by suppression of Ca++-dependent arrhythmogenic mechanisms, by direct reduction of pathologic Ca++ ov

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29

Anikin, G. S. "Pleiotropic features of dihydropyridine calcium channel antagonists." Systemic Hypertension 11, no. 3 (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 it

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30

Muralinath, E., Devi Pooja, Chbukdhara Prasanta, et al. "Understanding the Impact of Drugs on Cadmium Toxicity." Journal of Advances in Drug Discovery and Development 2, no. 1 (2023): 1–4. https://doi.org/10.5281/zenodo.10296990.

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<i>Cadmium is a heavy metal that exhibits significant health risks to humans and the environment. Exposure to cadmium can happen via different sources such as air, contaminated water and food. An accumulation of cadmium in tissues vand organs result in toxix effects. Chelation theory Is linked to the administration of chelating agents that bind to heavy metals namely cadmium and form complex compounds vthat can be eliminated from the body. DMSA (di mercantile succinic acid) and DMPS (2,3 mercpato _1_propane sulfonic acid ) are examples of chelating agents that result in a reduction of cadmium

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31

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 (1988): 176–86. http://dx.doi.org/10.1111/j.1749-6632.1988.tb33353.x.

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32

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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33

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

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34

Huguenard, John R. "Block of T-Type Ca²⁺ Channels Is an Important Action of Succinimide Antiabsence Drugs." Epilepsy Currents 2, no. 2 (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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35

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 (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 ce

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36

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 (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 isch

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37

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 enlargemen

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38

Rajeev, Prajapat, Chandra Shruti, and Singh Pooja. "Evaluation of Different Calcium Channel Blockers on Blood Glucose Level in Albino Rabbits." International Journal of Pharmaceutical and Clinical Research 15, no. 9 (2023): 413–17. https://doi.org/10.5281/zenodo.11344694.

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<strong>Background:</strong> Calcium channel blockers (CCBs) are a class of drugs and natural substances that disrupt the movement of calcium (Ca<sup>++</sup>) through calcium channels. The most widespread clinical use of calcium channel blockers is to decrease blood pressure in patients with hypertension, with particular efficacy in treating elderly patients. The present study was done to evaluate the effect of different CCB on blood glucose level in normal albino rabbits. <strong>Methods: </strong>The present study was conducted on healthy albino rabbits of either sex weighing

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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 (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 cha

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40

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 (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

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41

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 (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

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42

Almeshhadani, Mohammed Hasan, Khasro Adel Faeq, Kamal Mohammed Nidhamy, and Abdulsatar Kamil Faeq. "Assessment of the effects of antihypertensive drugs in patients suffering from hypertension in Kurdistan." Advanced medical journal 3, no. 2 (2017): 23–28. http://dx.doi.org/10.56056/amj.2017.27.

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Background and objectives: Hypertension is an important cardiovascular disease that carries a high rate of mortality and morbidity if not controlled. Significant complications of untreated hypertension include vascular atherosclerosis, chronic kidney diseases, and heart failure. The aim of this retrospective study is to improve practitioners' and specialists’ practices in the management of hypertension in the Kurdistan region. This study assesses the response of our local patient population to different first-line and combination therapies for hypertension to identify the most effective approa

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43

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 (2007): 207–12. http://dx.doi.org/10.1111/j.1559-4564.2007.06656.x.

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44

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

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45

Ozkul, Yasar. "Influence of calcium channel blocker drugs in neuromuscular transmission." Clinical Neurophysiology 118, no. 9 (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 (1985): B185—B195. http://dx.doi.org/10.1016/0002-9149(85)90630-7.

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Thammavongsa, Darani Ashley, Taylor N. Jackvony, Markus J. Bookland, and Min D. Tang-Schomer. "Targeting Ion Channels: Blockers Suppress Calcium Signals and Induce Cytotoxicity Across Medulloblastoma Cell Models." Bioengineering 12, no. 3 (2025): 268. https://doi.org/10.3390/bioengineering12030268.

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Medulloblastoma (MB) groups 3 and 4 lack targeted therapies despite their dismal prognoses. Ion channels and pumps have been implicated in promoting MB metastasis and growth; however, their roles remain poorly understood. In this study, we repurposed FDA-approved channel blockers and modulators to investigate their potential anti-tumor effects in MB cell lines (DAOY and D283) and primary cell cultures derived from a patient with MB. For the first time, we report spontaneous calcium signaling in MB cells. Spontaneous calcium signals were significantly reduced by mibefradil (calcium channel bloc

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Payandeh, Jian. "Crystallographic studies of voltage-gated sodium and calcium channels." Acta Crystallographica Section A Foundations and Advances 70, a1 (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

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Osadchuk, A. M., I. L. Davydkin, T. A. Gricenko, and M. A. Osadchuk. "Gastroesophageal reflux disease and esophagitis associated with the use of drugs: the modern state of the problem." Terapevticheskii arkhiv 91, no. 8 (2019): 135–40. http://dx.doi.org/10.26442/00403660.2019.08.000228.

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From the standpoint of evidence - based medicine, the ability of various drugs to induce the development of gastroesophageal reflux disease and esophagitis is considered. Thus, all known drugs can be divided into 3 groups: drugs that have the ability to reduce pressure in the lower esophageal sphincter, for example, β-adrenoreceptor agonists, α-adrenoreceptor antagonists, anticholinergics, calcium channel blockers, nitrates, benzodiazepines (diazepam), estrogen, progesterone, aminophylline (theophylline), tricyclic antidepressants, selective serotonin reuptake inhibitors, glucocorticosteroids;

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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 (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-boun

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