scholarly journals Inhibition of Ischemia-Induced Glutamate Release in Rat Striatum by Dihydrokinate and an Anion Channel Blocker

Stroke ◽  
1999 ◽  
Vol 30 (2) ◽  
pp. 433-440 ◽  
Author(s):  
Yukio Seki ◽  
Paul J. Feustel ◽  
Richard W. Keller ◽  
Bruce I. Tranmer ◽  
Harold K. Kimelberg
Keyword(s):  
Channel Blocker ◽  
Glutamate Release ◽  
Anion Channel ◽  
Rat Striatum ◽  
Anion Channel Blocker

Role of hydroxyl radical in superoxide induced microsomal lipid peroxidation: Protective effect of anion channel blocker

1996 ◽  
Vol 21 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Salil K. Ghosh ◽  
Tapati Chakraborti ◽  
Arun B. Banerjee ◽  
Sujata Roychoudhury ◽  
Sajal Chakraborti
Keyword(s):  
Lipid Peroxidation ◽  
Protective Effect ◽  
Hydroxyl Radical ◽  
Channel Blocker ◽  
Anion Channel ◽  
Microsomal Lipid Peroxidation ◽  
Anion Channel Blocker

scholarly journals Neuroprotective effects of volume-regulated anion channel blocker DCPIB on neonatal hypoxic-ischemic injury

2012 ◽  
Vol 34 (1) ◽  
pp. 113-118 ◽  
Author(s):  
Ammar Alibrahim ◽  
Li-yan Zhao ◽  
Christine You-jin Bae ◽  
Andrew Barszczyk ◽  
Christopher Lf Sun ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Ischemic Injury ◽  
Anion Channel ◽  
Neuroprotective Effects ◽  
Anion Channel Blocker ◽  
Hypoxic Ischemic Injury

Distinct Ca2+- and cAMP-dependent anion conductances in the apical membrane of polarized T84 cells

1998 ◽  
Vol 275 (2) ◽  
pp. C484-C495 ◽  
Author(s):  
Didier Merlin ◽  
Lianwei Jiang ◽  
Gregg R. Strohmeier ◽  
Asma Nusrat ◽  
Seth L. Alper ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Apical Membrane ◽  
Anion Channel ◽  
Epithelial Cell Line ◽  
T84 Cells ◽  
Cell Monolayers ◽  
Anion Conductance ◽  
Anion Selectivity ◽  
Colonic Epithelial Cell Line ◽  
Anion Channel Blocker

Monolayers of the human colonic epithelial cell line T84 exhibit electrogenic Cl− secretion in response to the Ca2+ agonist thapsigargin and to the cAMP agonist forskolin. To evaluate directly the regulation of apical Cl−conductance by these two agonists, we have utilized amphotericin B to permeabilize selectively the basolateral membranes of T84 cell monolayers. We find that apical anion conductance is stimulated by both forskolin and thapsigargin but that these conductances are differentially sensitive to the anion channel blocker DIDS. DIDS inhibits thapsigargin-stimulated responses completely but forskolin responses only partially. Furthermore, the apical membrane anion conductances elicited by these two agonists differ in anion selectivity (for thapsigargin, I− > Cl−; for forskolin, Cl− > I−). However, the DIDS-sensitive component of the forskolin-induced conductance response exhibits anion selectivity similar to that induced by thapsigargin (I− > Cl−). Thus forskolin-induced apical anion conductance comprises at least two components, one of which has features in common with that elicited by thapsigargin.

scholarly journals Secretion of acid and base equivalents by intact distal airways

2003 ◽  
Vol 284 (5) ◽  
pp. L855-L862 ◽  
Author(s):  
S. K. Inglis ◽  
S. M. Wilson ◽  
R. E. Olver
Keyword(s):  
Channel Blocker ◽  
Combined Treatment ◽  
Anion Channel ◽  
Potential Difference ◽  
Glandular Epithelium ◽  
Surface Epithelium ◽  
Glandular Secretion ◽  
Submucosal Glands ◽  
Acid And Base ◽  
Anion Channel Blocker

Secretion of HCO[Formula: see text] by airway submucosal glands is essential for normal liquid and mucus secretion. Because the liquid bathing the airway surface (ASL) is acidic, it has been proposed that the surface epithelium may acidify HCO[Formula: see text]-rich glandular fluid. The aim of this study was to investigate the mechanisms by which intact distal bronchi, which contain both surface and glandular epithelium, modify pH of luminal fluid. Distal bronchi were isolated from pig lungs, cannulated in a bath containing HCO[Formula: see text]-buffered solution, and perfused continually with an aliquot of similar, lightly buffered solution (LBS) in which NaCl replaced NaHCO[Formula: see text] (pH 7 with NaOH). The pH of this circulating LBS initially acidified (by 0.053 ± 0.0053 pH units) and transepithelial potential difference (PD) depolarized. The magnitude of acidification was increased when pHLBS was higher. This acidification was unaffected by luminal dimethylamiloride (DMA, 100 μM) but was inhibited by 100 nM bafilomycin A1 (by 76 ± 13%), suggesting involvement of vacuolar-H+ ATPase. Addition of ACh (10 μM) evoked alkalinization of luminal LBS and hyperpolarization of transepithelial PD. The alkalinization was inhibited in HCO[Formula: see text]-free solutions containing acetazolamide (1 mM) and by DMA and was enhanced by bumetanide (100 μM), an inhibitor of Cl− secretion. The hyperpolarization was unaffected by these maneuvers. The anion channel blocker 5-nitro-2-(3-phenylpropylamino)benzoate (300 μM) and combined treatment with DMA and bumetanide blocked both the alkalinization and hyperpolarization responses to ACh. These results are consistent with earlier studies showing that ACh evokes glandular secretion of HCO[Formula: see text] and Cl−. Isolated distal airways thus secrete both acid and base equivalents.

scholarly journals Selective role for superoxide in InsP3 receptor–mediated mitochondrial dysfunction and endothelial apoptosis

2005 ◽  
Vol 170 (7) ◽  
pp. 1079-1090 ◽  
Author(s):  
Muniswamy Madesh ◽  
Brian J. Hawkins ◽  
Tatyana Milovanova ◽  
Cunnigaiper D. Bhanumathy ◽  
Suresh K. Joseph ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Ischemia Reperfusion ◽  
Anion Channel ◽  
Ros Generation ◽  
Oxygen Species ◽  
Critical Function ◽  
Store Depletion ◽  
Anion Channel Blocker ◽  
Apoptotic Cascade ◽  
Insp3 Receptor

Reactive oxygen species (ROS) play a divergent role in both cell survival and cell death during ischemia/reperfusion (I/R) injury and associated inflammation. In this study, ROS generation by activated macrophages evoked an intracellular Ca2+ ([Ca2+]i) transient in endothelial cells that was ablated by a combination of superoxide dismutase and an anion channel blocker. [Ca2+]i store depletion, but not extracellular Ca2+ chelation, prevented [Ca2+]i elevation in response to O2.− that was inositol 1,4,5-trisphosphate (InsP3) dependent, and cells lacking the three InsP3 receptor (InsP3R) isoforms failed to display the [Ca2+]i transient. Importantly, the O2.−-triggered Ca2+ mobilization preceded a loss in mitochondrial membrane potential that was independent of other oxidants and mitochondrially derived ROS. Activation of apoptosis occurred selectively in response to O2.− and could be prevented by [Ca2+]i buffering. This study provides evidence that O2.− facilitates an InsP3R-linked apoptotic cascade and may serve a critical function in I/R injury and inflammation.

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