scholarly journals Background Nonselective Cationic Current and the Resting Membrane Potential in Rabbit Aorta Endothelial Cells.

2000 ◽  
Vol 50 (6) ◽  
pp. 635-643 ◽  
Author(s):  
Sung Jin Park ◽  
Young Chul Kim ◽  
Suk Hyo Suh ◽  
Hyewhon Rhim ◽  
Jae Hoon Sim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Rabbit Aorta ◽  
Resting Membrane Potential ◽  
Cationic Current ◽  
Nonselective Cationic Current

Metabolic communication from cardiac myocytes to vascular endothelial cells

2005 ◽  
Vol 288 (5) ◽  
pp. H2232-H2237 ◽  
Author(s):  
Anna K. Brzezinska ◽  
Daphne Merkus ◽  
William M. Chilian
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Cardiac Myocytes ◽  
Vascular Tone ◽  
Vascular Endothelial Cells ◽  
Resting Membrane Potential ◽  
Vascular Endothelial ◽  
Whole Cell ◽  
Cell Current ◽  
Whole Cell Current

The endothelium releases substances that affect both vascular and cardiac myocytes. However, under conditions of augmented metabolic demands and cardiac work, signals from the cardiac myocytes may be critical for the endothelium to fulfill its secretory and regulatory function in the vascular bed. Therefore, we hypothesized that cardiac myocytes produce substances that alter the resting membrane potential of endothelial cells and thus vascular tone. Isolated rat cardiac myocytes were electrically stimulated at the rate of 0 and 400 beats/min (Po2 = 150 mmHg), and supernatants were collected from each group (Sup-0; control) and (Sup-400) and used within 6 mo. These supernatants were applied to human coronary endothelial cells that were subsequently analyzed by using the whole cell and cell-attached patch-clamp modes. Sup-0 had no effect on the whole cell current and the zero-current potential. The Sup-0 from myocytes treated with aprotinin, an inhibitor of kallikrein and serine protease, reduced whole cell current between −120 and −60 mV. Sup-400 depolarized endothelial cells from the resting membrane potential of −45 to −5 mV ( P < 0.05), increased the magnitude of an inward current, and activated an outward current. Moreover, Sup-400 cells assayed in cell-attached patches increased single channel amplitude and the probability of a channel being in the open state. These effects were reversed by the Sup-400 from aprotinin-treated cells. We conclude that under certain metabolic conditions, isolated cardiac myocytes produce and release vasoactive substances that alter the function of K+ channels in vascular endothelial cells. Thus cardiac myocytes seem to communicate metabolic information to the endothelium, which could potentially influence vascular tone.

scholarly journals DIFFERENCES IN MEMBRANE POTENTIAL SENSITIVITY TO POTASSIUM CHANNEL OPENERS AND HYPOXIA BETWEEN INTACT AND CULTURED ENDOTHELIAL CELLS

2009 ◽  
Vol 55 (1) ◽  
pp. 49-56
Author(s):  
A.I. Bondarenko ◽  
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Cell Function ◽  
Cultured Cells ◽  
Rat Aorta ◽  
Resting Membrane Potential ◽  
Signaling Mechanism ◽  
Endothelial Cell Function ◽  
K Channels ◽  
Cultured Endothelial Cells

The influence of pinacidil, an activator of ATP-sensitive K+ channels, on the membrane potential of endothelial cells from intact rat aorta and cultured endothelial cells was investigated. Pinacidil evoked a slowly developing sustained hyperpolariza-tion of endothelial cells from isolated artery with the amplitude of 15±4 mV from the resting membrane potential of –4Ш мВ. In contrast, in cultured endothelial cells pinacidil was without response. Diazoxide, another activator of ATP-sensitive K+ channels, in half of the cultured cells tested, evoked a slowly developing sustained hyperpolarization with the amplitude of 3 mV. The rest of the cells studied did not respond by membrane potential changes to diazoxide. It was suggested that high sen­sitivity of the membrane potential of in situ endothelial cells to potassium channels openers may represent a potent signaling mechanism influencing endothelial cell function upon stimula­tion of vascular KATP channels.

scholarly journals Ca2+-activated K+ Channels in Murine Endothelial Cells: Block by Intracellular Calcium and Magnesium

2008 ◽  
Vol 131 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Jonathan Ledoux ◽  
Adrian D. Bonev ◽  
Mark T. Nelson
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Intracellular Calcium ◽  
Membrane Current ◽  
Mesenteric Arteries ◽  
Equilibrium Potential ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Additional Increase ◽  
K Channels

The intermediate (IKCa) and small (SKCa) conductance Ca2+-sensitive K+ channels in endothelial cells (ECs) modulate vascular diameter through regulation of EC membrane potential. However, contribution of IKCa and SKCa channels to membrane current and potential in native endothelial cells remains unclear. In freshly isolated endothelial cells from mouse aorta dialyzed with 3 μM free [Ca2+]i and 1 mM free [Mg2+]i, membrane currents reversed at the potassium equilibrium potential and exhibited an inward rectification at positive membrane potentials. Blockers of large-conductance, Ca2+-sensitive potassium (BKCa) and strong inward rectifier potassium (Kir) channels did not affect the membrane current. However, blockers of IKCa channels, charybdotoxin (ChTX), and of SKCa channels, apamin (Ap), significantly reduced the whole-cell current. Although IKCa and SKCa channels are intrinsically voltage independent, ChTX- and Ap-sensitive currents decreased steeply with membrane potential depolarization. Removal of intracellular Mg2+ significantly increased these currents. Moreover, concomitant reduction of the [Ca2+]i to 1 μM caused an additional increase in ChTX- and Ap-sensitive currents so that the currents exhibited theoretical outward rectification. Block of IKCa and SKCa channels caused a significant endothelial membrane potential depolarization (≈11 mV) and decrease in [Ca2+]i in mesenteric arteries in the absence of an agonist. These results indicate that [Ca2+]i can both activate and block IKCa and SKCa channels in endothelial cells, and that these channels regulate the resting membrane potential and intracellular calcium in native endothelium.

scholarly journals The interplay of seven subthreshold conductances controls the resting membrane potential and the oscillatory behavior of thalamocortical neurons

2014 ◽  
Vol 112 (2) ◽  
pp. 393-410 ◽  
Author(s):  
Yimy Amarillo ◽  
Edward Zagha ◽  
German Mato ◽  
Bernardo Rudy ◽  
Marcela S. Nadal
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Computational Model ◽  
Potassium Current ◽  
Brain Slices ◽  
Reversal Potential ◽  
Burst Firing ◽  
Resting Membrane Potential ◽  
Cationic Current ◽  
Steady State Current

The signaling properties of thalamocortical (TC) neurons depend on the diversity of ion conductance mechanisms that underlie their rich membrane behavior at subthreshold potentials. Using patch-clamp recordings of TC neurons in brain slices from mice and a realistic conductance-based computational model, we characterized seven subthreshold ion currents of TC neurons and quantified their individual contributions to the total steady-state conductance at levels below tonic firing threshold. We then used the TC neuron model to show that the resting membrane potential results from the interplay of several inward and outward currents over a background provided by the potassium and sodium leak currents. The steady-state conductances of depolarizing Ih (hyperpolarization-activated cationic current), IT (low-threshold calcium current), and INaP (persistent sodium current) move the membrane potential away from the reversal potential of the leak conductances. This depolarization is counteracted in turn by the hyperpolarizing steady-state current of IA (fast transient A-type potassium current) and IKir (inwardly rectifying potassium current). Using the computational model, we have shown that single parameter variations compatible with physiological or pathological modulation promote burst firing periodicity. The balance between three amplifying variables (activation of IT, activation of INaP, and activation of IKir) and three recovering variables (inactivation of IT, activation of IA, and activation of Ih) determines the propensity, or lack thereof, of repetitive burst firing of TC neurons. We also have determined the specific roles that each of these variables have during the intrinsic oscillation.

Synchronized Oscillations in the Inferior Olive Are Controlled by the Hyperpolarization-Activated Cation Current I h

1997 ◽  
Vol 77 (6) ◽  
pp. 3145-3156 ◽  
Author(s):  
Thierry Bal ◽  
David A. McCormick
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Inferior Olive ◽  
Local Application ◽  
Partial Replacement ◽  
Resting Membrane Potential ◽  
Pacemaker Potential ◽  
Cationic Current ◽  
Cation Current ◽  
Low Threshold

Bal, Thierry and David A. McCormick. Synchronized oscillations in the inferior olive are controlled by the hyperpolarization-activated cation current I h. J. Neurophysiol. 77: 3145–3156, 1997. The participation of a hyperpolarization-activated cationic current in the generation of oscillations in single inferior olive neurons and in the generation of ensemble oscillations in the inferior olive nucleus (IO) of the guinea pig and ferret was investigated in slices maintained in vitro. Intracellular recordings in guinea pig or ferret IO neurons revealed that these cells could generate sustained endogenous oscillations (4–10 Hz) at hyperpolarized membrane potentials (−60 to −67 mV) after the intracellular injection of a brief hyperpolarizing current pulse. These oscillations appeared as the rhythmic generation of a low-threshold Ca2+ spike that typically initiated one or two fast Na+-dependent action potentials. Between low-threshold Ca2+ spikes was an afterhyperpolarization that formed a “pacemaker” potential. Local application of apamin resulted in a large reduction in the amplitude of the afterhyperpolarization, indicating that a Ca2+-activated K+ current makes a strong contribution to its generation. However, even in the presence of apamin, hyperpolarization of IO neurons results in a “depolarizing sag” of the membrane potential that was blocked by local application of Cs+ or partial replacement of extracellular Na+ with choline+ or N-methyl-d-glucamine+, suggesting that I h also contributes to the generation of the afterhyperpolarization. Extracellular application of low concentrations of cesium resulted in hyperpolarization of the membrane potential of IO neurons and spontaneous 5- to 6-Hz oscillations in single, as well as networks, of IO neurons. Application of larger concentrations of cesium reduced the frequency of oscillation to 2–3 Hz or blocked the oscillation entirely. On the basis of these results, we propose that I h contributes to single and ensemble oscillations in the IO in two ways: 1) I h contributes to the determination of the resting membrane potential such that reduction of I h results in hyperpolarization of the membrane potential and an increased propensity of oscillation through removal of inactivation of the low-threshold Ca2+ current; and 2) I h contributes to the generation of the afterhyperpolarization and the pacemaker potential between low-threshold Ca2+ spikes.

Bethanidine increases one type of potassium current and relaxes aortic muscle

1988 ◽  
Vol 66 (6) ◽  
pp. 731-736 ◽  
Author(s):  
G. Bkaily ◽  
J.-P. Caillé ◽  
M. D. Payet ◽  
M. Peyrow ◽  
R. Sauvé ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Potassium Current ◽  
Single Cells ◽  
Rabbit Aorta ◽  
Cell Voltage ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Voltage Dependent

Using a whole-cell voltage-clamp technique, we identified two time- and voltage-dependent K+ currents: an early outward rectifier and a delayed outward rectifier in single vascular smooth muscle cells of rabbit aorta in culture. About 90% of the single cells tested showed a predominant delayed outward K+ current type. Both K+ currents were decreased by tetraethylammonium. In contrast, bethanidine sulphate (10−4 M), a pharmacological analog of the cardiac antifibrillatory drug, bretylium tosylate, decreased the early outward K+ current, increased the delayed rectifier K+ current type, and hyperpolarized the resting membrane potential. Bethanidine was found to relax vascular smooth muscle. The vasodilatory effect of bethanidine is associated with the activation of a K+ current that is probably involved in keeping the membrane potential at the resting state, thereby depressing the excitability of the aortic vascular smooth muscle.

Lysophosphatidylcholine Inhibits Receptor-Mediated Ca 2+ Mobilization in Intact Endothelial Cells of Rabbit Aorta

1997 ◽  
Vol 17 (8) ◽  
pp. 1561-1567 ◽  
Author(s):  
Yoichi Miwa ◽  
Ken-ichi Hirata ◽  
Seinosuke Kawashima ◽  
Hozuka Akita ◽  
Mitsuhiro Yokoyama
Keyword(s):  
Endothelial Cells ◽  
Rabbit Aorta
Sign in / Sign up

Export Citation Format

Share Document