scholarly journals Shaker-related voltage-gated K+channel expression and vasomotor function in human coronary resistance arteries

2018 ◽  
Vol 25 (1) ◽  
pp. e12431 ◽  
Author(s):  
Yoshinori Nishijima ◽  
Ankush Korishettar ◽  
Dawid S. Chabowski ◽  
Sheng Cao ◽  
Xiaodong Zheng ◽  
...  
Keyword(s):  
K Channel ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Voltage Gated ◽  
Vasomotor Function ◽  
Channel Expression

scholarly journals Impaired voltage-gated K+channel expression in brain during experimental cancer cachexia

FEBS Letters ◽  
2003 ◽  
Vol 536 (1-3) ◽  
pp. 45-50 ◽  
Author(s):  
Mireia Coma ◽  
Rubén Vicente ◽  
Silvia Busquets ◽  
Neus Carbó ◽  
Michael M Tamkun ◽  
...  
Keyword(s):  
Cancer Cachexia ◽  
K Channel ◽  
Voltage Gated ◽  
Experimental Cancer ◽  
Channel Expression

Voltage-gated K+-channel activity in ovine pulmonary vasculature is developmentally regulated

2000 ◽  
Vol 278 (6) ◽  
pp. L1297-L1304 ◽  
Author(s):  
David N. Cornfield ◽  
Connie B. Saqueton ◽  
Valerie A. Porter ◽  
Jean Herron ◽  
Ernesto Resnik ◽  
...  
Keyword(s):  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Developmental Changes ◽  
Pulmonary Vasculature ◽  
K Channel ◽  
Mrna Levels ◽  
Channel Activity ◽  
Developmentally Regulated ◽  
Voltage Gated ◽  
Channel Expression

To examine mechanisms underlying developmental changes in pulmonary vascular tone, we tested the hypotheses that 1) maturation-related changes in the ability of the pulmonary vasculature to respond to hypoxia are intrinsic to the pulmonary artery (PA) smooth muscle cells (SMCs); 2) voltage-gated K+(Kv)-channel activity increases with maturation; and 3) O2-sensitive Kv2.1 channel expression and message increase with maturation. To confirm that maturational differences are intrinsic to PASMCs, we used fluorescence microscopy to study the effect of acute hypoxia on cytosolic Ca2+concentration ([Ca2+]i) in SMCs isolated from adult and fetal PAs. Although PASMCs from both fetal and adult circulations were able to sense an acute decrease in O2 tension, acute hypoxia induced a more rapid and greater change in [Ca2+]i in magnitude in PASMCs from adult compared with fetal PAs. To determine developmental changes in Kv-channel activity, the effects of the K+-channel antagonist 4-aminopyridine (4-AP) were studied on fetal and adult PASMC [Ca2+]i. 4-AP (1 mM) caused PASMC [Ca2+]i to increase by 94 ± 22% in the fetus and 303 ± 46% in the adult. Kv-channel expression and mRNA levels in distal pulmonary arteries from fetal, neonatal, and adult sheep were determined through the use of immunoblotting and semiquantitative RT-PCR. Both Kv2.1-channel protein and mRNA expression in distal pulmonary vasculature increased with maturation. We conclude that there are maturation-dependent changes in PASMC O2 sensing that may render the adult PASMCs more responsive to acute hypoxia.

Hypoxia-induced hyperpolarization is not associated with vasodilation of bovine coronary resistance arteries

1997 ◽  
Vol 272 (3) ◽  
pp. H1462-H1469 ◽  
Author(s):  
K. M. Gauthier-Rein ◽  
D. M. Bizub ◽  
J. H. Lombard ◽  
N. J. Rusch
Keyword(s):  
Smooth Muscle ◽  
Salt Solution ◽  
Transmembrane Potential ◽  
Channel Blocker ◽  
K Channel ◽  
Physiological Salt Solution ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
K Channels ◽  
Channel Activator

The effect of reduced PO2 on the transmembrane potential and diameter of small cannulated coronary resistance arteries was evaluated by microelectrode and videomicroscopic methods. Bovine coronary resistance arteries (158 +/- 8 microm ID) were cannulated with glass micropipettes and perfused and superfused with physiological salt solution. Lowering the PO2 of the physiological salt solution from 140 +/- 4 to 36 +/- 2 mmHg increased the smooth muscle cell transmembrane potential from -51 +/- 2 to -62 +/- 2 mV in both endothelium-intact and -denuded coronary resistance arteries. This hyperpolarization was blocked by superfusion with the K+-channel blocker glibenclamide (1 microM). However, low PO2 did not significantly dilate either endothelium-intact or -denuded coronary resistance arteries, although superfusion with 1 microM cromakalim, a K+-channel activator, induced a 6-mV hyperpolarization and increased the diameter by 33 +/- 10 microm. These results suggest that reduced PO2 directly hyperpolarizes the vascular smooth muscle of coronary resistance arteries by activation of glibenclamide-sensitive K+ channels, but other nonvascular mechanisms may mediate the vasodilation response to low PO2.

scholarly journals Mitogen induction of ion channels in murine T lymphocytes.

1987 ◽  
Vol 89 (3) ◽  
pp. 405-420 ◽  
Author(s):  
T E Decoursey ◽  
K G Chandy ◽  
S Gupta ◽  
M D Cahalan
Keyword(s):  
T Lymphocytes ◽  
Time Course ◽  
K Channel ◽  
K Channels ◽  
Voltage Gated ◽  
Large Numbers ◽  
Predominant Type ◽  
Channel Expression ◽  
Activated T Lymphocytes ◽  
Cell Mitogen

Using gigohm-seal recording, we studied ion channel expression in resting and activated T lymphocytes from mice. Both the number of channels per cell and the predominant type of K+ channel depend upon the state of activation of the cell. Unstimulated T cells express small numbers of K+ channels, typically a dozen per cell, and are heterogeneous, usually expressing either type n or type l K+ channels (see DeCoursey, T. E., K. G. Chandy, S. Gupta, and M. D. Cahalan. 1987. Journal of General Physiology. 89:379-404). 1 d after stimulation by the murine T cell mitogen concanavalin A, large numbers of type n K+ channels appear in enlarged, activated cells. Type n channels appear in activated cells with a time course consistent with that reported for mitogen-induced enhancement of protein synthesis. Voltage-gated tetrodotoxin-sensitive Na+ channels present in about one-third of unstimulated cells from the MRL-n strain are increased approximately 10-fold after activation.

Endothelin-1 mediates hypoxia-induced inhibition of voltage-gated K+ channel expression in pulmonary arterial myocytes

2008 ◽  
Vol 294 (2) ◽  
pp. L309-L318 ◽  
Author(s):  
E. Miles Whitman ◽  
Sarah Pisarcik ◽  
Trevor Luke ◽  
Michele Fallon ◽  
Jian Wang ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Prolonged Exposure ◽  
Hypoxia Inducible Factor ◽  
K Channel ◽  
Channel Activity ◽  
Voltage Gated ◽  
Endothelin 1 ◽  
Voltage Dependent ◽  
Channel Expression ◽  
Pulmonary Arterial

Prolonged exposure to decreased oxygen tension causes contraction and proliferation of pulmonary arterial smooth muscle cells (PASMCs) and pulmonary hypertension. Hypoxia-induced inhibition of voltage-gated K+ (Kv) channels may contribute to the development of pulmonary hypertension by increasing intracellular calcium concentration ([Ca2+]i). The peptide endothelin-1 (ET-1) has been implicated in the development of pulmonary hypertension and acutely decreases Kv channel activity. ET-1 also activates several transcription factors, although whether ET-1 alters KV channel expression is unclear. The hypoxic induction of ET-1 is regulated by the transcription factor hypoxia-inducible factor-1 (HIF-1), which we demonstrated to regulate hypoxia-induced decreases in KV channel activity. In this study, we tested the hypothesis that HIF-1-dependent increases in ET-1 lead to decreased Kv channel expression and subsequent elevation in [Ca2+]i. Resting [Ca2+]i and Kv channel expression were measured in cells exposed to control (18% O2, 5% CO2) and hypoxic (4% O2, 5% CO2) conditions. Hypoxia caused a decrease in expression of Kv1.5 and Kv2.1 and a significant increase in resting [Ca2+]i. The increase in [Ca2+]i was reduced by nifedipine, an inhibitor of voltage-dependent calcium channels, and removal of extracellular calcium. Treatment with BQ-123, an ET-1 receptor inhibitor, prevented the hypoxia-induced decrease in Kv channel expression and blunted the hypoxia-induced increase in [Ca2+]i in PASMCs, whereas ET-1 mimicked the effects of hypoxia. Both hypoxia and overexpression of HIF-1 under normoxic conditions increased ET-1 expression. These results suggest that the inhibition of Kv channel expression and rise in [Ca2+]i during chronic hypoxia may be the result of HIF-1-dependent induction of ET-1.

scholarly journals A Xenopus oocyte model system to study action potentials

2018 ◽  
Vol 150 (11) ◽  
pp. 1583-1593 ◽  
Author(s):  
Aaron Corbin-Leftwich ◽  
Hannah E. Small ◽  
Helen H. Robinson ◽  
Carlos A. Villalba-Galea ◽  
Linda M. Boland
Keyword(s):  
Action Potentials ◽  
Subcellular Location ◽  
Model System ◽  
K Channel ◽  
Functional Coupling ◽  
Xenopus Laevis Oocytes ◽  
Excitable Cells ◽  
Voltage Gated ◽  
Channel Expression ◽  
Electrical Signaling

Action potentials (APs) are the functional units of fast electrical signaling in excitable cells. The upstroke and downstroke of an AP is generated by the competing and asynchronous action of Na+- and K+-selective voltage-gated conductances. Although a mixture of voltage-gated channels has been long recognized to contribute to the generation and temporal characteristics of the AP, understanding how each of these proteins function and are regulated during electrical signaling remains the subject of intense research. AP properties vary among different cellular types because of the expression diversity, subcellular location, and modulation of ion channels. These complexities, in addition to the functional coupling of these proteins by membrane potential, make it challenging to understand the roles of different channels in initiating and “temporally shaping” the AP. Here, to address this problem, we focus our efforts on finding conditions that allow reliable AP recordings from Xenopus laevis oocytes coexpressing Na+ and K+ channels. As a proof of principle, we show how the expression of a variety of K+ channel subtypes can modulate excitability in this minimal model system. This approach raises the prospect of studies on the modulation of APs by pharmacological or biological means with a controlled background of Na+ and K+ channel expression.

Influence of cloned voltage-gated K+ channel expression on alanine transport, Rb+ uptake, and cell volume

1993 ◽  
Vol 265 (5) ◽  
pp. C1230-C1238 ◽  
Author(s):  
A. Felipe ◽  
D. J. Snyders ◽  
K. K. Deal ◽  
M. M. Tamkun
Keyword(s):  
Membrane Potential ◽  
Atpase Activity ◽  
Cell Volume ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Wild Type ◽  
Transfected Cells ◽  
Voltage Gated ◽  
Alanine Transport ◽  
Channel Expression

Voltage-gated K+ channels are involved in regulation of action potential duration and in setting the resting membrane potential in nerve and muscle. To determine the effects of voltage-gated K+ channel expression on processes not associated with electrically excitable cells, we studied cell volume, membrane potential, Na(+)-K(+)-ATPase activity, and alanine transport after the stable expression of the Kv1.4 and Kv1.5 human K+ channels in Ltk- mouse fibroblasts (L-cells). The fast-activating noninactivating Kv1.5 channel, but not the rapidly inactivating Kv1.4 channel, prevented dexamethasone-induced increases in intracellular volume and inhibited Na(+)-K(+)-ATPase activity by 25%, as measured by 86Rb+ uptake. Alanine transport, measured separately by systems A and ASC, was lower in Kv1.5-expressing cells, indicating that the expression of this channel modified the Na(+)-dependent amino acid transport of both systems. Expression of the Kv1.4 channel did not alter alanine transport relative to wild-type or sham-transfected cells. The changes specific to Kv1.5 expression may be related to the resting membrane potential induced by this channel (-30 mV) in contrast to that measured in wild-type sham-transfected, or Kv1.4-transfected cells (-2 to 0 mV). Blocking of the Kv1.5 channel by 60 microM quinidine negated the effects of Kv1.5 expression on intracellular volume, Na(+)-K(+)-ATPase, and Na(+)-dependent alanine transport. These results indicate that delayed rectifier channels such as Kv1.5 can play a key role in the control of cell membrane potential, cell volume, Na(+)-K(+)-ATPase activity, and electrogenic alanine transport across the plasma membrane of electrically unexcitable cells.

scholarly journals Switch of Voltage-Gated K+ Channel Expression in the Plasma Membrane of Chondrogenic Cells Affects Cytosolic Ca2+-Oscillations and Cartilage Formation

PLoS ONE ◽  
2011 ◽  
Vol 6 (11) ◽  
pp. e27957 ◽  
Author(s):  
Zoltan Varga ◽  
Tamás Juhász ◽  
Csaba Matta ◽  
János Fodor ◽  
Éva Katona ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
K Channel ◽  
Voltage Gated ◽  
Cartilage Formation ◽  
Channel Expression ◽  
And Cartilage
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