Endothelial Cell K+ Channels, Membrane Potential and the Release of Vasoactive Factors from the Vascular Endothelium

2001 ◽  
pp. 667-689 ◽  
Author(s):  
Christopher R. Triggle
Keyword(s):  
Membrane Potential ◽  
Endothelial Cell ◽  
Vascular Endothelium ◽  
K Channels ◽  
Vasoactive Factors

scholarly journals Role of Ca+-dependent K-channels in the membrane potential and contractility of aorta from spontaneously hypertensive rats

1994 ◽  
Vol 113 (3) ◽  
pp. 1022-1028 ◽  
Author(s):  
Eneida G. Silva ◽  
Eugenio Frediani-Neto ◽  
Alice T. Ferreira ◽  
Antonio CM. Paiva ◽  
Therezinha B. Paiva
Keyword(s):  
Membrane Potential ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
K Channels

scholarly journals Expression of TASK and TREK, two-pore domain K+ channels, in human myometrium

Reproduction ◽  
2005 ◽  
Vol 129 (4) ◽  
pp. 525-530 ◽  
Author(s):  
Xilian Bai ◽  
George J Bugg ◽  
Susan L Greenwood ◽  
Jocelyn D Glazier ◽  
Colin P Sibley ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Pregnant Women ◽  
Human Myometrium ◽  
Rt Pcr ◽  
Excitable Cells ◽  
K Channels ◽  
Myometrial Cells ◽  
Channel Proteins ◽  
A Site ◽  
Pore Domain

Two-pore domain K+channels are an emerging family of K+channels that may contribute to setting membrane potential in both electrically excitable and non-excitable cells and, as such, influence cellular function. The human uteroplacental unit contains both excitable (e.g. myometrial) and non-excitable cells, whose function depends upon the activity of K+channels. We have therefore investigated the expression of two members of this family, TWIK (two-pore domain weak inward rectifying K+channel)-related acid-sensitive K+channel (TASK) and TWIK-related K+channel (TREK) in human myometrium. Using RT-PCR the mRNA expression of TASK and TREK isoforms was examined in myometrial tissue from pregnant women. mRNAs encoding TASK1, 4 and 5 and TREK1 were detected whereas weak or no signals were observed for TASK2, TASK3 and TREK2. Western blotting for TASK1 gave two bands of approximately 44 and 65 kDa, whereas TREK1 gave bands of approximately 59 and 90 kDa in myometrium from pregnant women. TASK1 and TREK1 immunofluorescence was prominent in intracellular and plasmalemmal locations within myometrial cells. Therefore, we conclude that the human myometrium is a site of expression for the two-pore domain K+channel proteins TASK1 and TREK1.

scholarly journals STUDIES ON ENDOTHELIAL REACTIONS

1920 ◽  
Vol 32 (5) ◽  
pp. 533-546 ◽  
Author(s):  
Nathan Chandler Foot
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelium ◽  
Colloidal Suspension ◽  
Giant Cells ◽  
Epithelioid Cell ◽  
Normal Lung ◽  
Capillary Endothelium ◽  
Alveolar Wall ◽  
Living Animal ◽  
Capillary Walls

1. The injection of a colloidal suspension, or sol, of carbon into the veins of a living animal, as recommended by McJunkin, furnishes an apparently reliable means of tracing the so called epithelioid cell of the pulmonary tubercle from its origin in the vascular endothelium to the lesion. 2. Experimental tubercles are formed in the lung, as in the liver, primarily by cells originating in the capillary endothelium. These cells are probably present in small numbers in the normal lung, lying free both in the alveolar wall and the air vesicles. In response to infection they proliferate in the capillary walls in the vicinity of the invading organisms, migrate in steadily increasing numbers, and, arriving at the site of the infection, further multiply and to some extent fuse to form the syncytia known as giant cells. 3. The epithelial cell takes no active part in the process; its proliferation tends to repair denuded surfaces and is regenerative rather than combative or phagocytic in nature. This cell is free from carbon and stains only diffusely with carmine, in contradistinction to the endothelial cell which readily takes up both pigments in granular form. 4. The cells of endothelial origin not only phagocytose tubercle bacilli, but carry them into the tissues, for example into lymph nodes, by way of the lymphatics, or into other lung lobules by way of the air passages, in which they are readily demonstrable.

scholarly journals Organ culture mimics the effects of hypoxia on membrane potential, K+ channels and vessel tone in pulmonary artery

2009 ◽  
Vol 158 (3) ◽  
pp. 848-861 ◽  
Author(s):  
Boris Manoury ◽  
Sarah L Etheridge ◽  
Joy Reid ◽  
Alison M Gurney
Keyword(s):  
Membrane Potential ◽  
Pulmonary Artery ◽  
Organ Culture ◽  
K Channels

scholarly journals Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Takamasa Kinoshita ◽  
Hiroyuki Tomita ◽  
Hideshi Okada ◽  
Ayumi Niwa ◽  
Fuminori Hyodo ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Heparan Sulfate ◽  
Vascular Endothelium ◽  
Wild Type ◽  
Brain Capillaries ◽  
Gene Encoding ◽  
Glioma Growth ◽  
Underlying Mechanisms ◽  
The Brain

Abstract Purpose Heparan sulfate (HS) is one of the factors that has been suggested to be associated with angiogenesis and invasion of glioblastoma (GBM), an aggressive and fast-growing brain tumor. However, it remains unclear how HS of endothelial cells is involved in angiogenesis in glioblastoma and its prognosis. Thus, we investigated the effect of endothelial cell HS on GBM development. Methods We generated endothelial cell-specific knockout of Ext1, a gene encoding a glycosyltransferase and essential for HS synthesis, and murine GL261 glioblastoma cells were orthotopically transplanted. Two weeks after transplantation, we examined the tumor progression and underlying mechanisms. Results The endothelial cell-specific Ext1 knockout (Ext1CKO) mice exhibited reduced HS expression specifically in the vascular endothelium of the brain capillaries compared with the control wild-type (WT) mice. GBM growth was significantly suppressed in Ext1CKO mice compared with that in WT mice. After GBM transplantation, the survival rate was significantly higher in Ext1CKO mice than in WT mice. We investigated how the effect of fibroblast growth factor 2 (FGF2), which is known as an angiogenesis-promoting factor, differs between Ext1CKO and WT mice by using an in vivo Matrigel assay and demonstrated that endothelial cell-specific HS reduction attenuated the effect of FGF2 on angiogenesis. Conclusions HS reduction in the vascular endothelium of the brain suppressed GBM growth and neovascularization in mice.

Inhibition of endothelium-dependent vasorelaxation by extracellular K+: a novel controlling signal for vascular contractility

2004 ◽  
Vol 286 (1) ◽  
pp. H329-H339 ◽  
Author(s):  
Geun Hee Seol ◽  
Seung Cheol Ahn ◽  
Ji Aee Kim ◽  
Bernd Nilius ◽  
Suk Hyo Suh
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Umbilical Vein ◽  
Vascular Contractility ◽  
Vasoactive Factors ◽  
Intracellular Ca ◽  
Prostaglandin F ◽  
Umbilical Vein Endothelial Cells ◽  
Mouse Aorta ◽  
Endothelium Dependent Relaxation

The effects of extracellular K+ on endothelium-dependent relaxation (EDR) and on intracellular Ca2+ concentration ([Ca2+]i) were examined in mouse aorta, mouse aorta endothelial cells (MAEC), and human umbilical vein endothelial cells (HUVEC). In mouse aortic rings precontracted with prostaglandin F2α or norepinephrine, an increase in extracellular K+ concentration ([K+]o) from 6 to 12 mM inhibited EDR concentration dependently. In endothelial cells, an increase in [K+]o inhibited the agonist-induced [Ca2+]i increase concentration dependently. Similar to K+, Cs+ also inhibited EDR and the increase in [Ca2+]i concentration dependently. In current-clamped HUVEC, increasing [K+]o from 6 to 12 mM depolarized membrane potential from –32.8 ± 2.7 to –8.6 ± 4.9 mV ( n = 8). In voltage-clamped HUVEC, depolarizing the holding potential from –50 to –25 mV decreased [Ca2+]i significantly from 0.95 ± 0.03 to 0.88 ± 0.03 μM ( n = 11, P < 0.01) and further decreased [Ca2+]i to 0.47 ± 0.04 μM by depolarizing the holding potential from –25 to 0 mV ( n = 11, P < 0.001). Tetraethylammonium (1 mM) inhibited EDR and the ATP-induced [Ca2+]i increase in voltage-clamped MAEC. The intermediate-conductance Ca2+-activated K+ channel openers 1-ethyl-2-benzimidazolinone, chlorozoxazone, and zoxazolamine reversed the K+-induced inhibition of EDR and increase in [Ca2+]i. The K+-induced inhibition of EDR and increase in [Ca2+]i was abolished by the Na+-K+ pump inhibitor ouabain (10 μM). These results indicate that an increase of [K+]o in the physiological range (6–12 mM) inhibits [Ca2+]i increase in endothelial cells and diminishes EDR by depolarizing the membrane potential, decreasing K+ efflux, and activating the Na+-K+ pump, thereby modulating the release of endothelium-derived vasoactive factors from endothelial cells and vasomotor tone.

Effect of pinacidil on ion permeability in resting and contracted resistance vessels

1990 ◽  
Vol 259 (1) ◽  
pp. H14-H22 ◽  
Author(s):  
L. M. Videbaek ◽  
C. Aalkjaer ◽  
A. D. Hughes ◽  
M. J. Mulvany
Keyword(s):  
Membrane Potential ◽  
Mechanism Of Action ◽  
Ion Permeability ◽  
K Channels ◽  
Complete Relaxation ◽  
Resistance Vessels ◽  
Flux Measurements ◽  
22Na Uptake ◽  
K Permeability ◽  
Cl Permeability

Pinacidil is thought to cause vasodilatation by opening K+ channels and consequent hyperpolarization. This proposed mechanism of action is based mainly on membrane potential measurements and 42K or 86Rb efflux experiments under resting conditions. We have measured the simultaneous effect of pinacidil on force and membrane potential in resting and norepinephrine-contracted rat mesenteric resistance vessels. Also the effect of pinacidil on 42K and 36Cl efflux and 22Na uptake in the absence and presence of norepinephrine was examined. From the membrane potential and ion flux measurements the ion permeabilities were calculated. In both resting and norepinephrine-contracted vessels, pinacidil caused a large hyperpolarization, the latter situation being associated with an almost complete relaxation. In both resting and norepinephrine-stimulated vessels, pinacidil caused a large increase in K+ permeability and a decrease in Cl-permeability, whereas no significant change of Na+ permeability was found. Our results suggest that pinacidil causes vasodilation due to hyperpolarization. The major cause for the hyperpolarization is an increase in K+ permeability.

Hyperkalemia alters EDHF-mediated hyperpolarization and relaxation in coronary arteries

1996 ◽  
Vol 271 (2) ◽  
pp. H760-H767 ◽  
Author(s):  
G. W. He ◽  
C. Q. Yang ◽  
W. F. Graier ◽  
J. A. Yang
Keyword(s):  
Nitric Oxide ◽  
Cardiac Surgery ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Organ Preservation ◽  
Maximal Response ◽  
K Channels ◽  
Porcine Coronary Artery ◽  
Preservation Solutions ◽  
Endothelium Dependent Relaxation

Hyperkalemic solutions are widely used to preserve organs for transplantation and for cardiac surgery. The present study was designed to test the hypothesis that hyperkalemia may alter endothelial function through a non-nitric oxide (NO) pathway, since preliminary studies have shown that the NO pathway may not be affected. Porcine coronary artery rings were studied in organ chambers. After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced. Incubation with hyperkalemia also significantly increased the concentration eliciting 50% of the maximal response to A23187 and bradykinin. A23187-induced hyperpolarization of the membrane potential was significantly reduced by hyperkalemic incubation. However, 1-h incubation with hyperkalemia does not affect the endothelial Ca2+ concentration. We conclude that exposure to hyperkalemia reduces the indomethacin- and L-NNA-resistant endothelium-dependent relaxation and endothelium-dependent hyperpolarization. This reduction in the relaxation and hyperpolarization is related to the endothelium-derived hyperpolarizing factor by affecting its effect on the smooth muscle cell, probably through partially depolarizing the membrane, and the Ca2(+)- activated K+ channels rather than by affecting its biosynthesis and/or release in the endothelial cell. Our study may suggest a new mechanism for coronary dysfunction after exposure to hyperkalemic cardioplegia and organ preservation solutions.

scholarly journals Distribution of sialoglycoconjugates on the luminal surface of the endothelial cell in the fenestrated capillaries of the pancreas.

1985 ◽  
Vol 33 (5) ◽  
pp. 474-476 ◽  
Author(s):  
V Muresan ◽  
M C Constantinescu
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelium ◽  
Binding Sites ◽  
Sodium Periodate ◽  
Luminal Surface ◽  
Nonspecific Binding ◽  
Coated Pits ◽  
Neuraminidase Treatment ◽  
Plasmalemmal Vesicles ◽  
Endothelial Surface

Sialic acid-bearing molecules on the luminal surface of the vascular endothelium in mouse and rat pancreatic capillaries were detected electron microscopically by using a procedure with ferritin hydrazide (FH), after preferential oxidation of sialyl residues with sodium periodate. The distribution of FH on the endothelial surface demonstrated the existence of microdomains with various densities of sialoglycoconjugates oxidizable by sodium periodate and accessible to the tracer. On the plasmalemma proper, FH binding sites were heterogeneously distributed. Their concentration on various microdomains decreased as follows: plasmalemma proper greater than coated pits greater than stomal diaphragms of plasmalemmal vesicles and transendothelial channels, and fenestral diaphragms. The membrane of plasmalemmal vesicles and transendothelial channels was not labeled by FH. Nonspecific binding of FH to the nonoxidized endothelial surface or that oxidized after neuraminidase treatment was relatively low.

The endothelial cell

2017 ◽  
Author(s):  
Ingrid Fleming ◽  
Brenda R. Kwak ◽  
Merlijn J. Meens
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Endothelium ◽  
Structural Heterogeneity ◽  
Physical Barrier ◽  
Physiological Functions

The endothelium, a monolayer of cells that lines blood vessels, acts as a physical barrier between circulating blood and vascular smooth muscle cells. The purpose of this chapter is to provide a general overview on the structural heterogeneity of the endothelium. Moreover, the most important physiological functions of the vascular endothelium in blood vessels are discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and hypertension, are provided in other chapters of this book.

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