Plasma membrane depolarization and activation of receptors for endogenous vasoconstrictors as possible mechanisms of potentiation of vasoconstrictive response to serotonin in traumatic shock in rats

2009 ◽  
Vol 36 (3) ◽  
pp. 285-297 ◽  
Author(s):  
L. M. Kozhevnikova ◽  
A. G. Davydova ◽  
P. V. Avdonin
Keyword(s):  
Plasma Membrane ◽  
Traumatic Shock ◽  
Membrane Depolarization

Oxidative burst and NO generation as initial response to ischemia in flow-adapted endothelial cells

2001 ◽  
Vol 280 (5) ◽  
pp. H2126-H2135 ◽  
Author(s):  
Yefim Manevich ◽  
Abu Al-Mehdi ◽  
Vladimir Muzykantov ◽  
Aron B. Fisher
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Oxidative Burst ◽  
Initial Response ◽  
Membrane Depolarization ◽  
No Synthase ◽  
Potential Production ◽  
Perfusion Chamber ◽  
Intracellular Ca ◽  
Static Conditions

Shear stress modulates endothelial physiology, yet the effect(s) of flow cessation is poorly understood. The initial metabolic responses of flow-adapted bovine pulmonary artery endothelial cells to the abrupt cessation of flow (simulated ischemia) was evaluated using a perfusion chamber designed for continuous spectroscopy. Plasma membrane potential, production of reactive O2 species (ROS), and intracellular Ca2+ and nitric oxide (NO) levels were measured with fluorescent probes. Within 15 s after flow cessation, flow-adapted cells, but not cells cultured under static conditions, showed plasma membrane depolarization and an oxidative burst with generation of ROS that was inhibited by diphenyleneiodonium. EGTA-inhibitable elevation of intracellular Ca2+ and NO were observed at ∼30 and 60 s after flow cessation, respectively. NO generation was decreased in the presence of inhibitors of NO synthase and calmodulin. Thus flow-adapted endothelial cells sense the altered hemodynamics associated with flow cessation and respond by plasma membrane depolarization, activation of NADPH oxidase, Ca2+ influx, and activation of Ca2+/calmodulin-dependent NO synthase. This signaling response is unrelated to cellular anoxia.

scholarly journals B cell activation. III. B cell plasma membrane depolarization and hyper-Ia antigen expression induced by receptor immunoglobulin cross-linking are coupled.

1983 ◽  
Vol 158 (5) ◽  
pp. 1589-1599 ◽  
Author(s):  
J G Monroe ◽  
J C Cambier
Keyword(s):  
Plasma Membrane ◽  
B Cells ◽  
B Cell ◽  
Cell Activation ◽  
Antigen Expression ◽  
Membrane Depolarization ◽  
Cell Surface Expression ◽  
Cross Linking ◽  
Cell Plasma Membrane ◽  
Cell Plasma

We report investigation of the relationship between ligand-induced B cell plasma membrane depolarization and increased expression of membrane-associated, I-A subregion encoded (mI-A) antigens. Results demonstrate that equal frequencies of B cells are stimulated to undergo membrane depolarization and to increase mI-A expression in response to mitogen, anti-Ig, and thymus-independent (TI) or thymus-dependent (TD) antigens. Further, a cause-and-effect relationship between these two events is suggested by results that demonstrate that inhibition of anti-Fab--induced depolarization by valinomycin also inhibits the subsequent increase in mI-A antigen expression and "passive" (non-ligand-mediated) depolarization of murine B cells by K+ results in hyper-mI-A antigen expression. Based upon these results we hypothesize that antigen-mediated receptor cross-linking results in signal transduction via membrane depolarization, which is resultant in increased mI-A antigen synthesis and cell surface expression. This increase in mI-A antigen density may render the B cell more receptive to subsequent interaction with I-region-restricted helper T cells.

Biochemical correlates of progesterone-induced plasma membrane depolarization during the first meiotic division inRana oocytes

1984 ◽  
Vol 77 (3) ◽  
pp. 201-212 ◽  
Author(s):  
Gene A. Morrill ◽  
David H. Ziegler ◽  
Jillian Kunar ◽  
Steven P. Weinstein ◽  
Adele B. Kostellow
Keyword(s):  
Plasma Membrane ◽  
Meiotic Division ◽  
Membrane Depolarization

Plasma membrane depolarization precedes photosynthesis damage and long-term leaf bleaching in (E)-chalcone-treated Arabidopsis shoots

2017 ◽  
Vol 218 ◽  
pp. 56-65 ◽  
Author(s):  
C. Díaz-Tielas ◽  
E. Graña ◽  
M.E. Maffei ◽  
M.J. Reigosa ◽  
A.M. Sánchez-Moreiras
Keyword(s):  
Plasma Membrane ◽  
Membrane Depolarization

scholarly journals Extracellular ATP activates different signalling pathways in rat Sertoli cells

1995 ◽  
Vol 311 (1) ◽  
pp. 269-274 ◽  
Author(s):  
C Foresta ◽  
M Rossato ◽  
P Bordon ◽  
F Di Virgilio
Keyword(s):  
Plasma Membrane ◽  
Pertussis Toxin ◽  
Sertoli Cells ◽  
Fluorescent Dyes ◽  
Purinergic Receptor ◽  
Membrane Depolarization ◽  
Extracellular Atp ◽  
Receptor Subtypes ◽  
Free Medium ◽  
Extracellular Medium

1. The present study describes effects of extracellular ATP (ATPe) on plasma membrane potential and cytoplasmic Ca2+ concentrations ([Ca2+]i) in rat Sertoli cells. Sertoli cells in suspension were stimulated with ATPe and other nucleotides and ionic changes were monitored utilizing the fluorescent dyes bis-oxonol and fura-2/AM. ATPe induced a prompt plasma membrane depolarization which was dependent on Na+ influx from the extracellular medium, since it was abolished by omission of extracellular Na+. Depolarization was independent of [Ca2+]i rise as it also occurred in the absence of extracellular Ca2+ and after intracellular Ca2+ stores were discharged with thapsigargin. ATPe also stimulated a rapid and biphasic increase in [Ca2+]i: a prompt spike was followed by a prolonged sustained plateau. The initial spike was dependent on Ca2+ release from intracellular stores since it was also present when cells were incubated in EGTA-supplemented Ca(2+)-free medium and was abolished by pretreatment with ionomycin and thapsigargin, agents that discharge intracellular Ca2+ stores. The sustained phase was dependent on Ca2+ influx from the extracellular medium as it was abolished when cells were incubated in EGTA-supplemented Ca(2+)-free medium. Ca2+ influx was due to activation of voltage-operated calcium channels (VOCCs) since it was abolished by the VOCC inhibitors verapamil and nifedipine or incubation in sucrose medium, an experimental condition which precludes plasma membrane depolarization by ATPe. 2. ATPe-induced rises in intracellular Ca2+ concentration and plasma membrane depolarization were reduced by pretreatment with pertussis toxin, suggesting that ATPe-activated transduction mechanisms are in part under the control of pertussis toxin-sensitive G-proteins. These data show that Sertoli cells possess P2-purinergic receptor subtypes coupled to influx of Na+ and release of Ca2+ from intracellular stores and provide evidence for an activation of different pathways by extracellular ATPe. Activation of these receptors induces Na+ influx that causes a rapid plasma membrane depolarization. Furthermore, ATPe also triggers Ca2+ release from intracellular stores and Ca2+ influx from extracellular space via dihydropyridine-sensitive VOCCs.

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