scholarly journals Membrane currents and the resting membrane potential in cultured bovine pulmonary artery endothelial cells.

1996 ◽  
Vol 497 (1) ◽  
pp. 95-107 ◽  
Author(s):  
T Voets ◽  
G Droogmans ◽  
B Nilius
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Membrane Currents ◽  
Resting Membrane Potential

Acute reductions in PO2 depolarize pulmonary artery endothelial cells and decrease [Ca2+]i

1994 ◽  
Vol 266 (4) ◽  
pp. H1416-H1421 ◽  
Author(s):  
T. Stevens ◽  
D. N. Cornfield ◽  
I. F. McMurtry ◽  
D. M. Rodman
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Driving Force ◽  
Primary Cultures ◽  
K Channel ◽  
Channel Blockers ◽  
Electrochemical Gradient ◽  
Similar Reduction ◽  
Fura 2

Whereas pulmonary artery endothelial cells (PAECs) are sensitive to oxygen, neither the effect of an acute reduction in PO2 on PAEC membrane potential nor its effect on intracellular free Ca2+ ([Ca2+]i) is known. We hypothesized that in confluent primary cultures of PAECs, an acute decrease in PO2 would depolarize the cell membrane, inhibit Ca2+ influx, and reduce [Ca2+]i. To test this hypothesis, the membrane-sensitive fluorophore bis (1,3-dibutylbarbituric acid) trimethine oxonol (DiBAC4, 1 microM) and [Ca2+]i-sensitive probe fura 2 (3 microM) were used. A decrease in PO2 from 125 to 35 mmHg caused membrane depolarization and a 60 +/- 8% (data are means +/- SE) reduction in Ca2+ influx, estimated by manganese quenching of fura 2 fluorescence. While basal [Ca2+]i was 79 +/- 5 nM in normoxic cells, it decreased to 31 +/- 2 nM after 15 min of hypoxia. Decreasing the electrochemical gradient for Ca2+ entry with either low extracellular Ca2+, the K+ channel blockers tetraethylammonium or charybdotoxin, or blockade of Ca2+ entry with lanthanum decreased [Ca2+]i by 54-71% of that observed during an acute reduction in PO2. These results demonstrate that an acute reduction in PO2 1) depolarizes PAECs, 2) reduces Ca2+ influx, and 3) decreases [Ca2+]i, and that a similar reduction in [Ca2+]i was observed with interventions designed to reduce the electrochemical driving force for Ca2+ entry.

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

Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells

2002 ◽  
Vol 283 (1) ◽  
pp. L120-L129 ◽  
Author(s):  
Eric Dubuis ◽  
Mathieu Gautier ◽  
Alexandre Melin ◽  
Manuel Rebocho ◽  
Catherine Girardin ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Outward Current ◽  
Muscle Cells ◽  
Membrane Resistance ◽  
Resting Membrane Potential ◽  
Whole Cell Patch Clamp

Exogenous carbon monoxide (CO) can induce pulmonary vasodilation by acting directly on pulmonary artery (PA) smooth muscle cells. We investigated the contribution of K+ channels to the regulation of resistance PA resting membrane potential on control (PAC) rats and rats exposed to CO for 3 wk at 530 parts/million, labeled as PACO rats. Whole cell patch-clamp experiments revealed that the resting membrane potential of PACO cells was more negative than that of PAC cells. This was associated with a decrease of membrane resistance in PACO cells. Additional analysis showed that outward current density in PACO cells was higher (50% at +60 mV) than in PAC cells. This was linked to an increase of iberiotoxin (IbTx)-sensitive current. Chronic CO hyperpolarized membrane of pressurized PA from −46.9 ± 1.2 to −56.4 ± 2.6 mV. Additionally, IbTx significantly depolarized membrane of smooth muscle cells from PACO arteries but not from PAC arteries. The present study provides initial evidence of an increase of Ca2+-activated K+ current in smooth muscle cells from PA of rats exposed to chronic CO.

Membrane properties of smooth muscle cells in pulmonary hypertensive rats

1982 ◽  
Vol 242 (5) ◽  
pp. H907-H915 ◽  
Author(s):  
H. Suzuki ◽  
B. M. Twarog
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Main Pulmonary Artery ◽  
Fold Increase ◽  
Muscle Cells ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Chronic Pulmonary Hypertension

The membrane properties of smooth muscle cells in rat main pulmonary artery (MPA) and small pulmonary artery (SPA) were investigated during chronic normobaric hypoxia and after monocrotaline injection. As chronic pulmonary hypertension developed, pronounced differences between MPA and SPA were observed. These findings may shed light on mechanisms of smooth muscle hypertrophy. 1) The resting membrane potential of smooth muscle in MPA became less negative than the normal (depolarized), whereas the resting membrane potential of smooth muscle in SPA became more negative (hyperpolarized). 2) In MPA, both the length and time constants diminished. 3) In MPA, the maximum membrane depolarization produced by a 10-fold increase in extracellular [K+] decreased. 4) In SPA, the depolarization observed in K+-free solution was more rapid and greater in amplitude, and the transient hyperpolarization following restoration of K+-containing solution increased. 5) In SPA, initial and sustained depolarization evoked by Na+-deficient solutions were increased. 6) Depolarization in MPA was due to increased membrane permeability, perhaps to Cl-, whereas hyperpolarization in SPA could be attributed to increased activity of an electrogenic Na+-K+ pump.

Effect of Bay K 8644 on tetraethylammonium-induced excitability of the rabbit pulmonary artery

1987 ◽  
Vol 65 (5) ◽  
pp. 828-833 ◽  
Author(s):  
Julia M. Ousterhout ◽  
Nick Sperelakis
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Action Potentials ◽  
Muscle Cells ◽  
Bay K 8644 ◽  
Resting Membrane Potential ◽  
Hypertonic Solution ◽  
Rabbit Pulmonary Artery

The effect of Bay K 8644 on the electrical activity of the smooth muscle cells in the main pulmonary artery of the rabbit was examined. In normal physiological solution, the resting membrane potential was −56 ± 0.6 mV, and the cells were electrically quiescent. Tetraethylammonium (5 mM) depolarized the membrane to about −45 mV, and electrical stimulation elicited action potentials. To suppress contractile responses and thereby facilitate sustained impalements, the muscle strips were bathed with a hypertonic solution containing sucrose. The mean amplitude of the tetraethylammonium-induced action potentials in the hypertonic solution was 35 ± 0.9 mV. The action potentials were dependent upon the extracellular Ca2+ concentration and were abolished by diltiazem (10−6 M). Spontaneous action potentials were occasionally generated in the presence of tetraethylammonium alone and could be induced by the further addition of Ba2+ (0.5 mM). The Ca2+ agonist Bay K 8644 (10−8 to 10−6 M) had no effect on the resting membrane potential or excitability in normal solution. However, in the hypertonic solution containing tetraethylammonium, Bay K 8644 caused a further depolarization and oscillatory potential changes, which were not prevented by tetrodotoxin. The oscillations were suppressed or abolished by diltiazem or nilvadipine. Thus, active responses can occur in the normally quiescent smooth muscle cells of the rabbit pulmonary artery when the outward K+ current(s) are suppressed.

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.

Modulation of mitochondrial Ca2+ by nitric oxide in cultured bovine vascular endothelial cells

2005 ◽  
Vol 289 (4) ◽  
pp. C836-C845 ◽  
Author(s):  
Elena N. Dedkova ◽  
Lothar A. Blatter
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Membrane Potential ◽  
Pulmonary Artery ◽  
Laser Scanning ◽  
Mitochondrial Permeability Transition ◽  
No Production ◽  
No Donor ◽  
Negative Feedback Regulation ◽  
Stimulation Of

In the present study, we used laser scanning confocal microscopy in combination with fluorescent indicator dyes to investigate the effects of nitric oxide (NO) produced endogenously by stimulation of the mitochondria-specific NO synthase (mtNOS) or applied exogenously through a NO donor, on mitochondrial Ca2+ uptake, membrane potential, and gating of mitochondrial permeability transition pore (PTP) in permeabilized cultured calf pulmonary artery endothelial (CPAE) cells. Higher concentrations (100–500 μM) of the NO donor spermine NONOate (Sper/NO) significantly reduced mitochondrial Ca2+ uptake and Ca2+ extrusion rates, whereas low concentrations of Sper/NO (<100 μM) had no effect on mitochondrial Ca2+ levels ([Ca2+]mt). Stimulation of mitochondrial NO production by incubating cells with 1 mM l-arginine also decreased mitochondrial Ca2+ uptake, whereas inhibition of mtNOS with 10 μM l- N5-(1-iminoethyl)ornithine resulted in a significant increase of [Ca2+]mt. Sper/NO application caused a dose-dependent sustained mitochondrial depolarization as revealed with the voltage-sensitive dye tetramethylrhodamine ethyl ester (TMRE). Blocking mtNOS hyperpolarized basal mitochondrial membrane potential and partially prevented Ca2+-induced decrease in TMRE fluorescence. Higher concentrations of Sper/NO (100–500 μM) induced PTP opening, whereas lower concentrations (<100 μM) had no effect. The data demonstrate that in calf pulmonary artery endothelial cells, stimulation of mitochondrial Ca2+ uptake can activate NO production in mitochondria that in turn can modulate mitochondrial Ca2+ uptake and efflux, demonstrating a negative feedback regulation. This mechanism may be particularly important to protect against mitochondrial Ca2+ overload under pathological conditions where cellular [NO] can reach very high levels.

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