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Journal articles on the topic 'K+-channels blockers'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Yaghi, Asma, Sanjay Mehta, and David G. McCormack. "Delayed rectifier potassium channels contribute to the depressed pulmonary artery contractility in pneumonia." Journal of Applied Physiology 93, no. 3 (2002): 957–65. http://dx.doi.org/10.1152/japplphysiol.01146.2001.

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We investigated the role of K+ channels in the attenuated pulmonary artery (PA) contractility characteristic of acute Pseudomonaspneumonia. Contractility of PA rings from the lungs of control or pneumonia rats was assessed in vitro by obtaining cumulative concentration-response curves to the contractile agonists KCl, phenylephrine, or PGF2α on PA rings before and after treatment with K+ channel blockers. In rings from pneumonia rats, paxilline (10 μM), tetraethylammonium (2 mM) (blockers of large-conductance Ca2+-activated K+ channels), and glybenclamide (ATP-sensitive K+ channel blocker, 80 μ

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2

Blaustein, Robert O. "Kinetics of Tethering Quaternary Ammonium Compounds to K+ Channels." Journal of General Physiology 120, no. 2 (2002): 203–16. http://dx.doi.org/10.1085/jgp.20028613.

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Polymeric maleimido–quaternary ammonium (QA) compounds have been shown to function as molecular tape measures when covalently tethered to external cysteine residues of a Shaker K+ channel (Blaustein R.O., P.A. Cole, C. Williams, and C. Miller. 2000. Nat. Struct. Biol. 7:309–311). For sufficiently long compounds, the cysteine–maleimide tethering reaction creates a high concentration, at the channel's pore, of a TEA-like moiety that irreversibly blocks current. This paper investigates a striking feature of the maleimide–cysteine tethering kinetics. Strong blockers—those that induce substantial l

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3

Wang, X., T. Inukai, M. A. Greer, and S. E. Greer. "Rat Prl and TSH secretion are regulated differently by K(+)-channel blockers." American Journal of Physiology-Endocrinology and Metabolism 266, no. 1 (1994): E39—E43. http://dx.doi.org/10.1152/ajpendo.1994.266.1.e39.

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All four different K(+)-channel blockers [tetraethylammonium (TEA), a nonselective K(+)-channel blocker; tolbutamide, an ATP-sensitive K(+)-channel blocker; quinine and 4-aminopyridine, both primarily voltage-dependent K(+)-channel blockers] stimulated prolactin (Prl) secretion by acutely dispersed anterior pituitary cells but had no effect on thyroid-stimulating hormone (TSH) secretion. TEA stimulated Prl secretion in a dose-dependent manner between 1 microM and 20 mM, but even as high as 20 mM, TEA did not induce TSH secretion. Valinomycin (2 microM), a K+ ionophore, inhibited both basal and

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4

Illek, B., H. Fischer, K. M. Kreusel, U. Hegel, and W. Clauss. "Volume-sensitive basolateral K+ channels in HT-29/B6 cells: block by lidocaine, quinidine, NPPB, and Ba2+." American Journal of Physiology-Cell Physiology 263, no. 3 (1992): C674—C683. http://dx.doi.org/10.1152/ajpcell.1992.263.3.c674.

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Volume-sensitive basolateral K+ channels were studied in apically amphotericin B-permeabilized HT-29/B6 monolayers in Ussing chambers with current fluctuation analysis. The basolateral K+ conductance and Lorentzian K+ channel noise were osmotically activated in presence of Cl- concentrations greater than or equal to 74 mM. Under isotonic conditions with 148 mM Cl-, a large transepithelial K+ current of 500 +/- 16.8 microA/cm2 and a spontaneous Lorentzian K+ channel noise with a corner frequency of 29.8 +/- 1.6 Hz (n = 31) were observed. Increasing extracellular osmolalities by addition of sucr

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5

Holmgren, Miguel, Paula L. Smith, and Gary Yellen. "Trapping of Organic Blockers by Closing of Voltage-dependent K+ Channels." Journal of General Physiology 109, no. 5 (1997): 527–35. http://dx.doi.org/10.1085/jgp.109.5.527.

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Small organic molecules, like quaternary ammonium compounds, have long been used to probe both the permeation and gating of voltage-dependent K+ channels. For most K+ channels, intracellularly applied quaternary ammonium (QA) compounds such as tetraethylammonium (TEA) and decyltriethylammonium (C10) behave primarily as open channel blockers: they can enter the channel only when it is open, and they must dissociate before the channel can close. In some cases, it is possible to force the channel to close with a QA blocker still bound, with the result that the blocker is “trapped.” Armstrong (J.

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6

Hill, Ceredwyn Elizabeth, and Jody Elisabeth Jacques. "Cholestatic effects of the K+ channel blockers Ba2+ and TEA occur through different pathways in the rat liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 1 (1999): G43—G48. http://dx.doi.org/10.1152/ajpgi.1999.276.1.g43.

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The role of K+ channels in bile acid-independent bile flow (BAIF) was studied in the isolated and bile duct-cannulated perfused rat liver by changing the driving force on K+and by using a variety of K+channel blockers. Bile flow rate, effluent perfusate K+ content, and portal pressure were measured. Increase in perfusate K+ from 5.9 to 80 mM caused inhibition of bile flow that could be fitted to a Boltzmann distribution, indicating partial dependence of bile formation on the K+ equilibrium potential and hence K+ channel activity. To investigate this further, the effects of compounds establishe

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7

Choi, Chang-Rok, Eun-Jin Kim, Tae Hyun Choi, Jaehee Han, and Dawon Kang. "Enhancing Human Cutaneous Wound Healing through Targeted Suppression of Large Conductance Ca2+-Activated K+ Channels." International Journal of Molecular Sciences 25, no. 2 (2024): 803. http://dx.doi.org/10.3390/ijms25020803.

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The modulation of K+ channels plays a crucial role in cell migration and proliferation, but the effect of K+ channels on human cutaneous wound healing (CWH) remains underexplored. This study aimed to determine the necessity of modulating K+ channel activity and expression for human CWH. The use of 25 mM KCl as a K+ channel blocker markedly improved wound healing in vitro (in keratinocytes and fibroblasts) and in vivo (in rat and porcine models). K+ channel blockers, such as quinine and tetraethylammonium, aided in vitro wound healing, while Ba2+ was the exception and did not show similar effec

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8

Artym, Vira V., та Howard R. Petty. "Molecular Proximity of Kv1.3 Voltage-gated Potassium Channels and β1-Integrins on the Plasma Membrane of Melanoma Cells". Journal of General Physiology 120, № 1 (2002): 29–37. http://dx.doi.org/10.1085/jgp.20028607.

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Tumor cell membranes have multiple components that participate in the process of metastasis. The present study investigates the physical association of β1-integrins and Kv1.3 voltage-gated potassium channels in melanoma cell membranes using resonance energy transfer (RET) techniques. RET between donor-labeled anti–β1-integrin and acceptor-labeled anti-Kv1.3 channels was detected on LOX cells adherent to glass and fibronectin-coated coverslips. However, RET was not observed on LOX cells in suspension, indicating that molecular proximity of these membrane molecules is adherence-related. Several

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9

Hur, Chang-Gi, Eun-Jin Kim, Seong-Keun Cho, et al. "K+ efflux through two-pore domain K+ channels is required for mouse embryonic development." REPRODUCTION 143, no. 5 (2012): 625–36. http://dx.doi.org/10.1530/rep-11-0225.

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Numerous studies have suggested that K+ channels regulate a wide range of physiological processes in mammalian cells. However, little is known about the specific function of K+ channels in germ cells. In this study, mouse zygotes were cultured in a medium containing K+ channel blockers to identify the functional role of K+ channels in mouse embryonic development. Voltage-dependent K+ channel blockers, such as tetraethylammonium and BaCl2, had no effect on embryonic development to the blastocyst stage, whereas K2P channel blockers, such as quinine, selective serotonin reuptake inhibitors (fluox

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10

Fujii, Naoto, Jeffrey C. Louie, Brendan D. McNeely, Tatsuro Amano, Takeshi Nishiyasu, and Glen P. Kenny. "Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: roles for KCa, KATP, and KV channels, nitric oxide, and prostanoids." Applied Physiology, Nutrition, and Metabolism 42, no. 5 (2017): 470–78. http://dx.doi.org/10.1139/apnm-2016-0615.

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We evaluated the influence of K+ channels (i.e., Ca2+-activated K+ (KCa), ATP-sensitive K+ (KATP), and voltage-gated K+ (KV) channels) and key enzymes (nitric oxide synthase (NOS) and cyclooxygenase (COX)) on nicotine-induced cutaneous vasodilation and sweating. Using intradermal microdialysis, we evaluated forearm cutaneous vascular conductance (CVC) and sweat rate in 2 separate protocols. In protocol 1 (n = 10), 4 separate sites were infused with (i) lactated Ringer (Control), (ii) 50 mmol·L−1 tetraethylammonium (KCa channel blocker), (iii) 5 mmol·L−1 glybenclamide (KATP channel blocker), an

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11

Martin-Eauclaire, Marie-France, and Pierre E. Bougis. "Potassium Channels Blockers from the Venom ofAndroctonus mauretanicus mauretanicus." Journal of Toxicology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/103608.

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K+channels selectively transport K+ions across cell membranes and play a key role in regulating the physiology of excitable and nonexcitable cells. Their activation allows the cell to repolarize after action potential firing and reduces excitability, whereas channel inhibition increases excitability. In eukaryotes, the pharmacology and pore topology of several structural classes of K+channels have been well characterized in the past two decades. This information has come about through the extensive use of scorpion toxins. We have participated in the isolation and in the characterization of sev

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12

Tagaya, E., J. Tamaoki, H. Takemura, and A. Nagai. "Regulation of adrenergic nerve-mediated contraction of canine pulmonary artery by K+ channels." European Respiratory Journal 11, no. 3 (1998): 571–74. http://dx.doi.org/10.1183/09031936.98.11030571.

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The aim of the present study was to investigate the role of certain subtypes of K+ channels in nerve-evoked contractions of pulmonary artery in vitro. The lobar or segmental pulmonary arteries were dissected from dogs, cut into ring segments, and the contractile responses to electrical field stimulation (EFS) and noradrenaline were measured under isometric conditions. Addition of iberiotoxin, a big conductance Ca2+-activated K+ channel blocker, and apamin, a small conductance Ca2+-activated K+ channel blocker, did not change the resting tension but augmented the contractile responses to EFS, s

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13

Nanda Kumar, N. S., Satish K. Singh, and Vazhaikkurichi M. Rajendran. "Mucosal potassium efflux mediated via Kcnn4 channels provides the driving force for electrogenic anion secretion in colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 3 (2010): G707—G714. http://dx.doi.org/10.1152/ajpgi.00101.2010.

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Intermediate conductance K+ (Kcnn4) channels are present in both mucosal and serosal membranes of colon. However, only serosal Kcnn4 channels have been shown to be essential for agonist-induced (cAMP and Ca2+) anion secretion. The present study sought to determine whether mucosal Kcnn4 channels also play a role in colonic anion secretion. Mucosal-to-serosal and serosal-to-mucosal unidirectional 86Rb (K+ surrogate) fluxes as well as short-circuit current ( Isc; a measure of anion secretion) were measured under voltage-clamp conditions in distal colon from rats fed either a standard or K+-free d

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14

Ortiz, Mario I., Raquel Cariño-Cortés, Víctor M. Muñoz-Pérez, Carlo Eduardo Medina-Solís, and Gilberto Castañeda-Hernández. "Citral inhibits the nociception in the rat formalin test: effect of metformin and blockers of opioid receptor and the NO-cGMP-K⁺ channel pathway." Canadian Journal of Physiology and Pharmacology 100, no. 4 (2022): 306–13. http://dx.doi.org/10.1139/cjpp-2021-0458.

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The objective of the present study was to scrutinize the effect of nitric oxide (NO), cyclic GMP (cGMP), potassium channel blockers, and metformin on the citral-produced peripheral antinociception. The rat paw 1% formalin test was used to assess nociception and antinociception. Rats were treated with local peripheral administration of citral (10–100 µg/paw). The antinociception of citral (100 µg/paw) was evaluated with and without the local pretreatment of naloxone, NG-L-nitro-arginine methyl ester (L-NAME, a NO synthesis inhibitor), 1H-(1,2,4)-oxadiazolo(4,2-a)quinoxalin-1-one (ODQ, a soluble

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15

Funabashi, Kenji, Susumu Ohya, Hisao Yamamura, et al. "Accelerated Ca2+ entry by membrane hyperpolarization due to Ca2+-activated K+ channel activation in response to histamine in chondrocytes." American Journal of Physiology-Cell Physiology 298, no. 4 (2010): C786—C797. http://dx.doi.org/10.1152/ajpcell.00469.2009.

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In articular cartilage inflammation, histamine release from mast cells is a key event. It can enhance cytokine production and matrix synthesis and also promote cell proliferation by stimulating chondrocytes. In this study, the functional impact of Ca2+-activated K+ (KCa) channels in the regulation of intracellular Ca2+ concentration ([Ca2+]i) in chondrocytes in response to histamine was examined using OUMS-27 cells, as a model of chondrocytes derived from human chondrosarcoma. Application of histamine induced a significant [Ca2+]i rise and also membrane hyperpolarization, and both effects were

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16

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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17

Chow, L. W. C., K. S. Cheng, K. L. Wong, and Y. M. Leung. "Voltage-Gated K+ Channels Promote BT-474 Breast Cancer Cell Migration." Journal of Global Oncology 4, Supplement 2 (2018): 192s. http://dx.doi.org/10.1200/jgo.18.79301.

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Objective: A variety of ion channels have been implicated in breast cancer proliferation and metastasis. Voltage-gated K+ (Kv) channels not only cause repolarization in excitable cells, but are also involved in multiple cellular functions in nonexcitable cells. In this study we investigated the role of Kv channels in migration of BT474 breast cancer cells. Methods: Transwell technique was used to separate migratory cells from nonmigratory ones and these 2 groups of cells were subject to electrophysiological examinations and microfluorimetric measurements for cytosolic Ca2+. Cell migration was

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18

Zhou, Ben-Yuan, Wei Ma, and Xin-Yun Huang. "Specific Antibodies to the External Vestibule of Voltage-gated Potassium Channels Block Current." Journal of General Physiology 111, no. 4 (1998): 555–63. http://dx.doi.org/10.1085/jgp.111.4.555.

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Using delayed-rectifier potassium channels as examples, we have designed two specific blockers by generating specific antipeptide antibodies to epitopes in the external vestibules of two channel proteins, Kv1.2 and Kv3.1. These antibodies reduced whole-cell Kv1.2 or Kv3.1 currents in transfected cells and the effect was blocked by the corresponding peptide antigen, but not by control peptides. A control antibody had little effect on Kv1.2 currents and the Kv1.2 blocker antibody had limited effect on other related potassium currents. Furthermore, the Kv1.2 blocking antibody inhibited dendrotoxi

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19

Wolfs, Jef L., Simone J. Wielders, Paul Comfurius, et al. "Reversible inhibition of the platelet procoagulant response through manipulation of the Gardos channel." Blood 108, no. 7 (2006): 2223–28. http://dx.doi.org/10.1182/blood-2006-01-009613.

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Abstract The platelet procoagulant response requires a sustained elevation of the intracellular Ca2+ concentration, [Ca2+]i, causing exposure of phosphatidylserine (PS) at the outer surface of the plasma membrane. An increased [Ca2+]i also activates Ca2+-dependent K+ channels. Here, we investigated the contribution of the efflux of K+ ions on the platelet procoagulant response in collagen-thrombin–activated platelets using selective K+ channel blockers. The Gardos channel blockers clotrimazol, charybdotoxin, and quinine caused a similar decrease in prothrombinase activity as well as in the num

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Higashimori, Haruki, Víctor M. Blanco, Vengopal Raju Tuniki, John R. Falck, and Jessica A. Filosa. "Role of epoxyeicosatrienoic acids as autocrine metabolites in glutamate-mediated K+ signaling in perivascular astrocytes." American Journal of Physiology-Cell Physiology 299, no. 5 (2010): C1068—C1078. http://dx.doi.org/10.1152/ajpcell.00225.2010.

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Epoxyeicosatrienoic acids (EETs), synthesized and released by astrocytes in response to glutamate, are known to play a pivotal role in neurovascular coupling. In vascular smooth muscle cells (VSMC), EETs activate large-conductance, Ca2+-activated K+ (BK) channels resulting in hyperpolarization and vasodilation. However, the functional role and mechanism of action for glial-derived EETs are still to be determined. In this study, we evaluated the effect of the synthetic EET analog 11-nonyloxy-undec-8(Z)-enoic acid (NUD-GA) on outward K+ currents mediated by calcium-activated K+ channels. Additio

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Wang, Jun, Shigeru Morishima, and Yasunobu Okada. "IK channels are involved in the regulatory volume decrease in human epithelial cells." American Journal of Physiology-Cell Physiology 284, no. 1 (2003): C77—C84. http://dx.doi.org/10.1152/ajpcell.00132.2002.

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Parallel activation of Ca2+-dependent K+ channels and volume-sensitive Cl− channels is known to be responsible for KCl efflux during regulatory volume decrease (RVD) in human epithelial Intestine 407 cells. The present study was performed to identify the K+ channel type. RT-PCR demonstrated mRNA expression of Ca2+-activated, intermediate conductance K+(IK), but not small conductance K+ (SK1) or large conductance K+ (BK) channels in this cell line. Whole cell recordings showed that ionomycin or hypotonic stress activated inwardly rectifying K+ currents that were reversibly blocked by IK channel

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Sidell, N., L. C. Schlichter, S. C. Wright, S. Hagiwara, and S. H. Golub. "Potassium channels in human NK cells are involved in discrete stages of the killing process." Journal of Immunology 137, no. 5 (1986): 1650–58. http://dx.doi.org/10.4049/jimmunol.137.5.1650.

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Abstract Using the whole-cell variation of the patch-clamp technique, we have found a voltage-dependent K+ current in human natural killer (NK) cells. This K+ current is reduced in a dose-dependent manner by a variety of ion-channel blockers (verapamil, quinidine, 4-aminopyridine, Cd2+) at concentrations comparable to those that inhibit natural killing. Pretreatment of target cells with quinidine or verapamil did not significantly reduce their sensitivity to killing, whereas substantial inhibition of killing was observed after pretreatment of effector cells. Both verapamil and quinidine reduce

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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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Rosenbaum, Tamara, Ariela Gordon-Shaag, León D. Islas, Jeremy Cooper, Mika Munari, and Sharona E. Gordon. "State-dependent Block of CNG Channels by Dequalinium." Journal of General Physiology 123, no. 3 (2004): 295–304. http://dx.doi.org/10.1085/jgp.200308925.

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Cyclic nucleotide–gated (CNG) ion channels are nonselective cation channels with a high permeability for Ca2+. Not surprisingly, they are blocked by a number of Ca2+ channel blockers including tetracaine, pimozide, and diltiazem. We studied the effects of dequalinium, an extracellular blocker of the small conductance Ca2+-activated K+ channel. We previously noted that dequalinium is a high-affinity blocker of CNGA1 channels from the intracellular side, with little or no state dependence at 0 mV. Here we examined block by dequalinium at a broad range of voltages in both CNGA1 and CNGA2 channels

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Geng, Yanyan, Xiaoyu Wang, and Karl L. Magleby. "Lack of negative slope in I-V plots for BK channels at positive potentials in the absence of intracellular blockers." Journal of General Physiology 141, no. 4 (2013): 493–97. http://dx.doi.org/10.1085/jgp.201210955.

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Large-conductance, voltage- and Ca2+-activated K+ (BK) channels display near linear current–voltage (I-V) plots for voltages between −100 and +100 mV, with an increasing sublinearity for more positive potentials. As is the case for many types of channels, BK channels are blocked at positive potentials by intracellular Ca2+ and Mg2+. This fast block progressively reduces single-channel conductance with increasing voltage, giving rise to a negative slope in the I-V plots beyond about +120 mV, depending on the concentration of the blockers. In contrast to these observations of pronounced differen

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Kawasaki, Keisuke, Yoshiaki Suzuki, Hisao Yamamura, and Yuji Imaizumi. "Development of a Novel Cell-Based Assay System for High-Throughput Screening of Compounds Acting on Background Two-Pore Domain K+ Channels." SLAS DISCOVERY: Advancing the Science of Drug Discovery 24, no. 6 (2019): 641–52. http://dx.doi.org/10.1177/2472555219829745.

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Two-pore domain K+ (K2P) channels are thought to be druggable targets. However, only a few agents specific for K2P channels have been identified, presumably due to the lack of an efficient screening system. To develop a new high-throughput screening (HTS) system targeting these channels, we have established a HEK293-based “test cell” expressing a mutated Na+ channel (Nav1.5) with markedly slowed inactivation, as well as a K+ channel (Kir2.1) that sets the membrane potential quite negative, close to K+ equilibrium potential. We found in this system that Kir2.1 block by 100 μM Ba2+ application c

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Reeve, Helen L., E. Kenneth Weir, Stephen L. Archer, and David N. Cornfield. "A maturational shift in pulmonary K+ channels, from Ca2+ sensitive to voltage dependent." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 6 (1998): L1019—L1025. http://dx.doi.org/10.1152/ajplung.1998.275.6.l1019.

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The mechanism responsible for the abrupt decrease in resistance of the pulmonary circulation at birth may include changes in the activity of O2-sensitive K+ channels. We characterized the electrophysiological properties of fetal and adult ovine pulmonary arterial (PA) smooth muscle cells (SMCs) using conventional and amphotericin B-perforated patch-clamp techniques. Whole cell K+ currents of fetal PASMCs in hypoxia were small and characteristic of spontaneously transient outward currents. The average resting membrane potential (RMP) was −36 ± 3 mV and could be depolarized by charybdotoxin (100

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Sultan, Sabena, Martin Gosling, Shadi Abu-Hayyeh, Nessa Carey, and Janet T. Powell. "Flow-dependent increase of ICAM-1 on saphenous vein endothelium is sensitive to apamin." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (2004): H22—H28. http://dx.doi.org/10.1152/ajpheart.00880.2003.

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The potassium channel blocker tetraethylammonium blocks the flow-induced increase in endothelial ICAM-1. We have investigated the subtype of potassium channel that modulates flow-induced increased expression of ICAM-1 on saphenous vein endothelium. Cultured human saphenous vein endothelial cells (HSVECs) or intact saphenous veins were perfused at fixed low and high flows in a laminar shear chamber or flow rig, respectively, in the presence or absence of potassium channel blockers. Expression of K+ channels and endothelial ICAM-1 was measured by real-time polymerase chain reaction and/or immuno

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Gomez-Niño, Angela, Ana Obeso, Jose Antonio Baranda, Jaime Santo-Domingo, Jose Ramon Lopez-Lopez, and Constancio Gonzalez. "MaxiK potassium channels in the function of chemoreceptor cells of the rat carotid body." American Journal of Physiology-Cell Physiology 297, no. 3 (2009): C715—C722. http://dx.doi.org/10.1152/ajpcell.00507.2008.

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Hypoxia activates chemoreceptor cells of the carotid body (CB) promoting an increase in their normoxic release of neurotransmitters. Catecholamine (CA) release rate parallels the intensity of hypoxia. Coupling of hypoxia to CA release requires cell depolarization, produced by inhibition of O2-regulated K+ channels, and Ca2+ entering the cells via voltage-operated channels. In rat chemoreceptor cells hypoxia inhibits large-conductance, calcium-sensitive K channels (maxiK) and a two-pore domain weakly inward rectifying K+ channel (TWIK)-like acid-sensitive K+ channel (TASK)-like channel, but the

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Ravens, Ursula. "Atrial-selective K+ channel blockers: potential antiarrhythmic drugs in atrial fibrillation?" Canadian Journal of Physiology and Pharmacology 95, no. 11 (2017): 1313–18. http://dx.doi.org/10.1139/cjpp-2017-0024.

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In the wake of demographic change in Western countries, atrial fibrillation has reached an epidemiological scale, yet current strategies for drug treatment of the arrhythmia lack sufficient efficacy and safety. In search of novel medications, atrial-selective drugs that specifically target atrial over other cardiac functions have been developed. Here, I will address drugs acting on potassium (K+) channels that are either predominantly expressed in atria or possess electrophysiological properties distinct in atria from ventricles. These channels include the ultra-rapidly activating, delayed out

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Guggino, S. E., W. B. Guggino, N. Green, and B. Sacktor. "Blocking agents of Ca2+-activated K+ channels in cultured medullary thick ascending limb cells." American Journal of Physiology-Cell Physiology 252, no. 2 (1987): C128—C137. http://dx.doi.org/10.1152/ajpcell.1987.252.2.c128.

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Ca2+-activated K+ channels with estimated single channel conductances of 127 +/- 2 pS were identified in the apical cell membrane of clone A3 of cultured medullary thick ascending limb (MTAL) cells. Both Ba2+ and the scorpion toxin, charybdotoxin (CTX), are slow blockers of the channels. An application of 0.1 microM Ba2+ to the intracellular face caused a 50% reduction in fractional open time (fv). Ba2+ block is both concentration and voltage dependent. Concentrations of CTX as low as 2 nM in the extracellular solution caused a significant reduction in fv. Tetraethylammonium (TEA) and quinine

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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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Zhang, L., A. D. Bonev, M. T. Nelson, and G. M. Mawe. "Ionic basis of the action potential of guinea pig gallbladder smooth muscle cells." American Journal of Physiology-Cell Physiology 265, no. 6 (1993): C1552—C1561. http://dx.doi.org/10.1152/ajpcell.1993.265.6.c1552.

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Smooth muscle cells in the intact guinea pig gallbladder had a resting membrane potential of about -45 mV and had spontaneous action potentials that consisted of a rapid depolarization, a transient repolarization, a plateau phase, and a complete repolarization. These action potentials lasted approximately 570 ms and occurred at a frequency of approximately 0.4 Hz. Action potentials were abolished by the dihydropyridine (DHP)-sensitive Ca2+ channel blocker nifedipine (1.0 microM) and were enhanced by the DHP-sensitive Ca2+ channel agonist BAY K 8644 (0.5 microM). The K+ channel blockers tetraet

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Hayashi, Mikio, Jing Wang, Susanne E. Hede, and Ivana Novak. "An intermediate-conductance Ca2+-activated K+ channel is important for secretion in pancreatic duct cells." American Journal of Physiology-Cell Physiology 303, no. 2 (2012): C151—C159. http://dx.doi.org/10.1152/ajpcell.00089.2012.

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Potassium channels play a vital role in maintaining the membrane potential and the driving force for anion secretion in epithelia. In pancreatic ducts, which secrete bicarbonate-rich fluid, the identity of K+ channels has not been extensively investigated. In this study, we investigated the molecular basis of functional K+ channels in rodent and human pancreatic ducts (Capan-1, PANC-1, and CFPAC-1) using molecular and electrophysiological techniques. RT-PCR analysis revealed mRNAs for KCNQ1, KCNH2, KCNH5, KCNT1, and KCNT2, as well as KCNN4 coding for the following channels: KVLQT1; HERG; EAG2;

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Tenma, Taro, Hirofumi Mitsuyama, Masaya Watanabe, et al. "Small-conductance Ca2+-activated K+ channel activation deteriorates hypoxic ventricular arrhythmias via CaMKII in cardiac hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (2018): H262—H272. http://dx.doi.org/10.1152/ajpheart.00636.2017.

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The molecular and electrophysiological mechanisms of acute ischemic ventricular arrhythmias in hypertrophied hearts are not well known. We hypothesized that small-conductance Ca2+-activated K+ (SK) channels are activated during hypoxia via the Ca2+/calmodulin-dependent protein kinase II (CaMKII)-dependent pathway. We used normotensive Wistar-Kyoto (WKY) rats and spontaneous hypertensive rats (SHRs) as a model of cardiac hypertrophy. The inhibitory effects of SK channels and ATP-sensitive K+ channels on electrophysiological changes and genesis of arrhythmias during simulated global hypoxia (GH)

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Upadhyay-Dhungel, K., CJ Kim, and A. Dhungel. "Magnesium induced vascular relaxation and role of Calcium-dependent K+ Channels." Janaki Medical College Journal of Medical Science 1, no. 1 (2013): 9–13. http://dx.doi.org/10.3126/jmcjms.v1i1.7880.

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Background and objectives: Magnesium is established as a neuro-protective agent and now also known as a vasodilator. It has been known for treating vasospasm following subarachnoid hemorrhage. However, its action mechanism in cerebral vascular relaxation is not clear. Potassium channels play a pivotal role in the relaxation of smooth muscle cells. To investigate their role in magnesium-induced relaxation of basilar smooth muscle cells, we examined the effect of magnesium on potassium channels using the patch clamp technique on cells from rabbit basilar artery. Material and Methods: Fresh smoot

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Hempelmann, Ralf G., Jörg Seebeck, Albrecht Ziegler, and H. Maximilian Mehdorn. "Effects of potassium channel inhibitors on the relaxation induced by the NO donor DEA/NO in isolated human cerebral arteries." Journal of Neurosurgery 93, no. 6 (2000): 1048–54. http://dx.doi.org/10.3171/jns.2000.93.6.1048.

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Object. The goal of this study was to investigate whether K+ channels are involved in nitric oxide (NO)—induced relaxation of isolated human cerebral arteries.Methods. Successive concentration—response curves relating to the use of the NO donor diethylamine NO (DEA/NO) were established in the absence and presence of different K+ channel inhibitors after mounting human cerebral arteries onto a wire myograph. The arteries were obtained from macroscopically intact tissue that had been removed during brain tumor operations.A high K+ concentration partially inhibited the relaxant effects of DEA/NO.

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Pék-Scott, Marta, and Peter L. Lutz. "ATP-sensitive K+ channel activation provides transient protection to the anoxic turtle brain." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 6 (1998): R2023—R2027. http://dx.doi.org/10.1152/ajpregu.1998.275.6.r2023.

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There is wide speculation that ATP-sensitive K+(KATP) channels serve a protective function in the mammalian brain, being activated during periods of energy failure. The aim of the present study was to determine if KATP channels also have a protective role in the anoxia-tolerant turtle brain. After ouabain administration, rates of change in extracellular K+ were measured in the telencephalon of normoxic and anoxic turtles ( Trachemys scripta). The rate of K+ efflux was reduced by 50% within 1 h of anoxia and by 70% at 2 h of anoxia, and no further decrease was seen at 4 h of anoxia. The additio

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Seth, Vikas, Mushtaq Ahmad, Prerna Upadhyaya, Monika Sharma, and Vijay Moghe. "Effect of Potassium Channel Modulators on Morphine Withdrawal in Mice." Substance Abuse: Research and Treatment 4 (January 2010): SART.S6211. http://dx.doi.org/10.4137/sart.s6211.

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The present study was conducted to investigate the effect of potassium channel openers and blockers on morphine withdrawal syndrome. Mice were rendered dependent on morphine by subcutaneous injection of morphine; four hours later, withdrawal was induced by using an opioid antagonist, naloxone. Mice were observed for 30 minutes for the withdrawal signs ie, the characteristic jumping, hyperactivity, urination and diarrhea. ATP-dependent potassium (K+ATP) channel modulators were injected intraperitoneally (i.p.) 30 minutes before the naloxone. It was found that a K+ATP channel opener, minoxidil (

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Vanelli, G., H. Y. Chang, A. G. Gatensby, and S. N. Hussain. "Contribution of potassium channels to active hyperemia of the canine diaphragm." Journal of Applied Physiology 76, no. 3 (1994): 1098–105. http://dx.doi.org/10.1152/jappl.1994.76.3.1098.

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Glibenclamide, iberiotoxin, and apamin (blockers of ATP-sensitive, large-conductance, and small-conductance Ca(2+)-activated K+ channels, respectively) were infused into the diaphragmatic vasculature of anesthetized indomethacin-treated dogs to assess the contribution of K+ channels to active hyperemia. Diaphragmatic blood flow (Qphr) and O2 uptake (VO2di) were measured at rest and during 2 min of continuous left phrenic nerve stimulation at 0.5, 1, 2, and 4 Hz. These measurements were repeated before (control) and after the infusion of a selective K+ channel blocker in three groups of animals

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Walsh, Kenneth B. "Screening Technologies for Inward Rectifier Potassium Channels: Discovery of New Blockers and Activators." SLAS DISCOVERY: Advancing the Science of Drug Discovery 25, no. 5 (2020): 420–33. http://dx.doi.org/10.1177/2472555220905558.

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K+ channels play a critical role in maintaining the normal electrical activity of excitable cells by setting the cell resting membrane potential and by determining the shape and duration of the action potential. In nonexcitable cells, K+ channels establish electrochemical gradients necessary for maintaining salt and volume homeostasis of body fluids. Inward rectifier K+ (Kir) channels typically conduct larger inward currents than outward currents, resulting in an inwardly rectifying current versus voltage relationship. This property of inward rectification results from the voltage-dependent bl

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Xie, Yaxia, Elke Zacharias, Patricia Hoff, and Frank Tegtmeier. "Ion Channel Involvement in Anoxic Depolarization Induced by Cardiac Arrest in Rat Brain." Journal of Cerebral Blood Flow & Metabolism 15, no. 4 (1995): 587–94. http://dx.doi.org/10.1038/jcbfm.1995.72.

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Anoxic depolarization (AD) and failure of ion homeostasis play an important role in ischemia-induced neuronal injury. In the present study, different drugs with known ion-channel-modulating properties were examined for their ability to interfere with cardiac-arrest-elicited AD and with the changes in the extracellular ion activity in rat brain. Our results indicate that only drugs primarily blocking membrane Na+ permeability (NBQX, R56865, and flunarizine) delayed the occurrence of AD, while compounds affecting cellular Ca2+ load (MK-801 and nimodipine) did not influence the latency time. The

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Yu, Y. M., F. Lermioglu, and A. Hassid. "Modulation of Ca by agents affecting voltage-sensitive Ca channels in mesangial cells." American Journal of Physiology-Renal Physiology 257, no. 6 (1989): F1094—F1099. http://dx.doi.org/10.1152/ajprenal.1989.257.6.f1094.

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The purpose of this study was to investigate the effects of depolarizing media and of Ca-channel activators and blockers on cytosolic free Ca in cultured rat mesangial cells. Membrane depolarizing media, containing 10–100 mM K+, dose dependently increased cytosolic Ca, and this effect was sustained and reversible. Nifedipine and lanthanum ion inhibited this increase, whereas verapamil was ineffective. A Ca-channel activator, BAY K 8644, dose dependently increased resting Ca levels, and nifedipine inhibited this effect. Moreover, the increase of Ca induced by maximally effective high K+ and BAY

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Wu, Lingyun, Zunzhe Wang, and Rui Wang. "Tetraethylammonium-evoked oscillatory contractions of rat tail artery: A K-K model." Canadian Journal of Physiology and Pharmacology 78, no. 9 (2000): 696–707. http://dx.doi.org/10.1139/y00-041.

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Spontaneously rhythmic contraction of peripheral blood vessels actively modulates the peripheral circulation and blood pressure. However, the underlying mechanisms for the complex rhythmic contraction patterns of various vascular tissues are not yet fully understood. In the present study, the tetraethylammonium (TEA)-induced spontaneously oscillatory contractions of isolated rat tail artery tissues were examined. It was found that TEA evoked arterial oscillatory contractions in a concentration-dependent, but endothelium-independent manner. The voltage- dependent K+ (Kv) channel specific blocke

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Geary, G. G., D. N. Krause, and S. P. Duckles. "Melatonin directly constricts rat cerebral arteries through modulation of potassium channels." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 3 (1997): H1530—H1536. http://dx.doi.org/10.1152/ajpheart.1997.273.3.h1530.

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The pineal hormone melatonin was found to decrease luminal diameter of rat middle cerebral artery segments, pressurized in vitro, in a concentration-dependent manner (concentration that produced a half-maximal effect = 2.7 nM). Contractile responses to melatonin were inhibited by luzindole, a melatonin receptor antagonist, but not by the serotonin receptor antagonist ketanserin. Pertussis toxin abolished the effect of melatonin, which is consistent with involvement of Gi or G(o) protein-coupled receptors. The maximal effect of melatonin was increased by elevating transmural pressure. When comp

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Kurjak, M., A. Sennefelder, M. Aigner, V. Schusdziarra, and H. D. Allescher. "Characterizing voltage-dependent Ca2+ channels coupled to VIP release and NO synthesis in enteric synaptosomes." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 5 (2002): G1027—G1034. http://dx.doi.org/10.1152/ajpgi.00400.2001.

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In enteric synaptosomes of the rat, the role of voltage-dependent Ca2+channels in K+-induced VIP release and nitric oxide (NO) synthesis was investigated. Basal VIP release was 39 ± 4 pg/mg, and cofactor-substituted NO synthase activity was 7.0 ± 0.8 fmol · mg−1 · min−1. K+ depolarization (65 mM) stimulated VIP release Ca2+ dependently (basal, 100%; K+, 172.2 ± 16.2%; P < 0.05, n = 5). K+-stimulated VIP release was reduced by blockers of the P-type (ω-agatoxin-IVA, 3 × 10−8 M) and N-type (ω-conotoxin-GVIA, 10−6 M) Ca2+ channels by ∼50 and 25%, respectively, but not by blockers of the L-type

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Bratz, Ian N., Gregory M. Dick, L. Donald Partridge та Nancy L. Kanagy. "Reduced molecular expression of K+ channel proteins in vascular smooth muscle from rats made hypertensive with Nω-nitro-l-arginine". American Journal of Physiology-Heart and Circulatory Physiology 289, № 3 (2005): H1277—H1283. http://dx.doi.org/10.1152/ajpheart.01052.2004.

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Smooth muscle membrane potential ( Em) depends on K+ channels, and arteries from rats made hypertensive with Nω-nitro-l-arginine (LHR) are depolarized compared with control. We hypothesized that decreased K+ channel function, due to decreased K+ channel protein expression, underlies Em depolarization. Furthermore, K+ channel blockers should move control Em (−46 ± 1 mV) toward that in LHR (−37 ± 2 mV) and normalize contraction. The Em vs. K+ relationship was less steep in LHR (23 ± 2 vs. 28 ± 1 mV/log K+ concentration), and contractile sensitivity to K+ was increased (EC50 = 37 ± 1 vs. 23 ± 1 m

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Gati, Christiano D. C., Márcia R. Mortari, and Elisabeth F. Schwartz. "Towards Therapeutic Applications of Arthropod VenomK+-Channel Blockers in CNS Neurologic Diseases Involving Memory Acquisition and Storage." Journal of Toxicology 2012 (2012): 1–21. http://dx.doi.org/10.1155/2012/756358.

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Potassium channels are the most heterogeneous and widely distributed group of ion channels and play important functions in all cells, in both normal and pathological mechanisms, including learning and memory processes. Being fundamental for many diverse physiological processes, K+-channels are recognized as potential therapeutic targets in the treatment of several Central Nervous System (CNS) diseases, such as multiple sclerosis, Parkinson's and Alzheimer's diseases, schizophrenia, HIV-1-associated dementia, and epilepsy. Blockers of these channels are therefore potential candidates for the sy

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Jepps, Thomas A., Iain A. Greenwood, James D. Moffatt, Kenton M. Sanders, and Susumu Ohya. "Molecular and functional characterization of Kv7 K+ channel in murine gastrointestinal smooth muscles." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 1 (2009): G107—G115. http://dx.doi.org/10.1152/ajpgi.00057.2009.

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Members of the Kv7 voltage-gated K+ channel family are important determinants of cardiac and neuronal membrane excitability. Recently, we and others have shown that Kv7 channels are also crucial regulators of smooth muscle activity. The aim of the present study was to assess the Kv7 expression in different parts of the murine gastrointestinal (GI) tract and to assess their functional roles by use of pharmacological agents. Of KCNQ/Kv7 members, both KCNQ4/Kv7.4 and KCNQ5/Kv7.5 genes and proteins were the most abundantly expressed Kv7 channels in smooth muscles throughout the GI tract. Immunohis

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Troncoso Brindeiro, Carmen M., Rachel W. Fallet, Pascale H. Lane, and Pamela K. Carmines. "Potassium channel contributions to afferent arteriolar tone in normal and diabetic rat kidney." American Journal of Physiology-Renal Physiology 295, no. 1 (2008): F171—F178. http://dx.doi.org/10.1152/ajprenal.00563.2007.

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We previously reported an enhanced tonic dilator impact of ATP-sensitive K+ channels in afferent arterioles of rats with streptozotocin (STZ)-induced diabetes. The present study explored the hypothesis that other types of K+ channel also contribute to afferent arteriolar dilation in STZ rats. The in vitro blood-perfused juxtamedullary nephron technique was utilized to quantify afferent arteriolar lumen diameter responses to K+ channel blockers: 0.1–3.0 mM 4-aminopyridine (4-AP; KV channels), 10–100 μM barium (KIR channels), 1–100 nM tertiapin-Q (TPQ; Kir1.1 and Kir3.x subfamilies of KIR channe

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