scholarly journals Glycyrrhetinic derivatives inhibit hyperpolarization in endothelial cells of guinea pig and rat arteries

2002 ◽  
Vol 282 (1) ◽  
pp. H335-H341 ◽  
Author(s):  
Marianne Tare ◽  
H. A. Coleman ◽  
Helena C. Parkington
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Resting Membrane Potential ◽  
Variable Effect

Glycyrrhetinic acid (GA) derivatives have been used to implicate gap junctions in vasorelaxation attributed to endothelium-derived hyperpolarizing factor (EDHF). The aim of this study was to assess whether GA compounds affect endothelial cell hyperpolarization. Membrane potentials were recorded from dye-identified endothelial and smooth muscle cells of guinea pig coronary and rat mesenteric arteries. GA derivatives had varied effects on the resting membrane potential: depolarization, hyperpolarization, or no effect, depending on the artery. 18α-GA (50 μM) had a small variable effect on ACh-induced hyperpolarizations in endothelial cells. 18β-GA (30 μM) and carbenoxolone (100 μM) significantly reduced ACh-induced hyperpolarizations in both endothelial and smooth muscle cells. Smooth muscle action potentials in rat tail arteries were smaller and slower in the presence of 18β-GA. Nerve-induced excitatory junction potentials were inhibited by 18β-GA and carbenoxolone, whereas the time course of their decay initially increased and then decreased. In conclusion, the GA compounds had a range of effects. Their inhibition of the EDHF hyperpolarization and relaxation in the smooth muscle may stem from the inhibition of endothelial cell hyperpolarization.

Voltage-dependent calcium channel current in isolated gallbladder smooth muscle cells of guinea pig

1993 ◽  
Vol 264 (6) ◽  
pp. G1066-G1076 ◽  
Author(s):  
T. Shimada
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Reversal Potential ◽  
High Sensitivity ◽  
Muscle Cells ◽  
Patch Clamp Technique ◽  
Decay Component ◽  
Voltage Dependent

The voltage-dependent Ca2+ current was studied in enzymatically dispersed guinea pig gallbladder smooth muscle cells using the whole cell patch-clamp technique. Depolarizing voltage (V) steps induced an inward current (I) that was carried by Ca2+. The threshold potential was -40 to -30 mV, the maximal current was observed at +10 to +20 mV, and the reversal potential was around +80 mV. I-V curves obtained with holding potentials of -80 and -40 mV were not significantly different. This current had a high sensitivity to dihydropyridine drugs, and the Ba2+ or Sr2+ current was larger than the Ca2+ current. Activation was accelerated by increasing the membrane potential. In general, the time course of decay was well fitted by the sum of two exponentials, but consideration of a third (ultra-slow) decay component was also necessary when the current generated by a 2-s command pulse was analyzed. Superimposition of activation and inactivation curves showed the presence of a significant window current. Carbachol suppressed the Ca2+ current only when the pipette contained a low concentration of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. These results show that the L-type Ca2+ current is dominant in gallbladder smooth muscle cells and may contribute to excitation-contraction coupling.

Electrical activation of endothelium evokes vasodilation and hyperpolarization along hamster feed arteries

2001 ◽  
Vol 280 (1) ◽  
pp. H160-H167 ◽  
Author(s):  
Geoffrey G. Emerson ◽  
Steven S. Segal
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Cell Damage ◽  
Muscle Cells ◽  
Sympathetic Nerves ◽  
Retractor Muscle ◽  
Receptor Interactions ◽  
Feed Arteries

Endothelial cells are considered electrically unexcitable. However, endothelium-dependent vasodilators (e.g., acetylcholine) often evoke hyperpolarization. We hypothesized that electrical stimulation of endothelial cells could evoke hyperpolarization and vasodilation. Feed artery segments (resting diameter: 63 ± 1 μm; length 3–4 mm) of the hamster retractor muscle were isolated and pressurized to 75 mmHg, and focal stimulation was performed via microelectrodes positioned across one end of the vessel. Stimulation at 16 Hz (30–50 V, 1-ms pulses, 5 s) evoked constriction (−20 ± 2 μm) that spread along the entire vessel via perivascular sympathetic nerves, as shown by inhibition with tetrodotoxin, ω-conotoxin, or phentolamine. In contrast, stimulation with direct current (30 V, 5 s) evoked vasodilation (16 ± 2 μm) and hyperpolarization (11 ± 1 mV) of endothelial and smooth muscle cells that conducted along the entire vessel. Conducted responses were insensitive to preceding treatments, atropine, or N ω-nitro-l-arginine, yet were abolished by endothelial cell damage (with air). Injection of negative current (≤1.6 nA) into a single endothelial cell reproduced vasodilator responses along the entire vessel. We conclude that, independent of ligand-receptor interactions, endothelial cell hyperpolarization evokes vasodilation that is readily conducted along the vessel wall. Moreover, electrical events originating within a single endothelial cell can drive the relaxation of smooth muscle cells throughout the entire vessel.

Changes in resting membrane potential induced by active sensitization in the guinea-pig vas deferens

1998 ◽  
Vol 76 (7-8) ◽  
pp. 802-806 ◽  
Author(s):  
J Noireaud ◽  
O Souilem ◽  
S Baudet ◽  
J -C Bidon ◽  
M Gogny ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Vas Deferens ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Resting Membrane Potential ◽  
Ouabain Binding

Smooth muscles hyperresponsiveness is a common feature in anaphylaxis and allergic diseases. The aim of the present work was to investigate whether the enhanced reactivity of sensitized guinea-pig vas deferens was associated with changes in the resting membrane potential (Er) of the smooth muscle cells. Active sensitization was performed by subcutaneous injection of egg albumen. Er was measured in vitro in isolated vas deferens with conventional KCl-filled microelectrodes. Quantification of [3H]ouabain binding sites, measurements of 86Rb efflux, and measurements of Na and K contents were also performed. In normal physiological solution, at 35°C, Er was a mean of -54.1 ± 0.3 mV (mean ± SEM) in control vas deferens. Sensitization resulted in depolarizing Er by about 7 mV. In control and sensitized preparations, the 3H-ouabain binding site concentration, the efflux of 86Rb, and the K content were similar. In guinea-pig vas deferens, active sensitization induced a partial depolarization of the resting membrane potential of the smooth muscle cells, which did not result from a downregulation of Na+-K+ pump sites.Key words: hyperreactivity, sensitization, Na+-K+ ATPase, guinea-pig, vas deferens, smooth muscle.

scholarly journals An endothelial cell-derived growth factor.

1980 ◽  
Vol 85 (2) ◽  
pp. 467-472 ◽  
Author(s):  
C Gajdusek ◽  
P DiCorleto ◽  
R Ross ◽  
S M Schwartz
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Platelet Derived Growth Factor ◽  
3T3 Cells ◽  
Free Plasma ◽  
Heat Instability

Cell-free plasma-derived serum (PDS) is deficient in the platelet-derived growth factor and will not support the growth of 3T3 cells, fibroblasts, or smooth muscle cells. However, when PDS-containing medium is preincubated with endothelial cells, the medium becomes modified so that it will support growth. The activity produced by the endothelial cells results from a polypeptide of 10,000 to 30,000 daltons which has several features that differ from those of the platelet-derived growth factor, including heat instability and lack of adsorption to CM Sephadex.

Freeze-Etch Studies on the Innervation of Mesenteric Arteries and Vas Deferens

1971 ◽  
Vol 9 (2) ◽  
pp. 411-425
Author(s):  
C. E. DEVINE ◽  
F. O. SIMPSON ◽  
W. S. BERTAUD
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Schwann Cells ◽  
Synaptic Vesicles ◽  
Vas Deferens ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Axonal Membrane ◽  
Freeze Etching

The innervation of mesenteric arteries and vas deferens of guinea-pig and vas deferens of mouse was examined by freeze-etching. Axons in bundles at large distances from the smooth muscle cells, were invested by Schwann cells and contained mainly neurotubules, while axons close to the smooth muscle cells had varicosities up to 1.6 µm in diameter and 2.0 µm long containing mainly small (approximately 50 nm) and large (approximately 100 nm) synaptic vesicles. Vascular axons differed from those in the vas deferens in that the former were at the medial adventitial border with an observed closest neuromuscular distance of approximately 200 nm and the latter were between smooth muscle cells at distances of 20-50 nm. Depressions of the axonal surface were seen and particles up to 15 nm were found on the axonal membrane.

Time course of Ca2+-dependent K+ and Cl− currents in single smooth muscle cells of guinea-pig trachea

1996 ◽  
Vol 306 (1-3) ◽  
pp. 227-236 ◽  
Author(s):  
Satoshi Henmi ◽  
Yuji Imaizumi ◽  
Katsuhiko Muraki ◽  
Minoru Watanabe
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Muscle Cells

Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles

2007 ◽  
Vol 292 (4) ◽  
pp. F1124-F1131 ◽  
Author(s):  
T. R. Uhrenholt ◽  
J. Schjerning ◽  
P. M. Vanhoutte ◽  
B. L. Jensen ◽  
O. Skøtt
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Calcium Sensitivity ◽  
No Production ◽  
Contractile Apparatus ◽  
Afferent Arterioles

Vasoconstriction and increase in the intracellular calcium concentration ([Ca2+]i) of vascular smooth muscle cells may cause an increase of endothelial cell [Ca2+]i, which, in turn, augments nitric oxide (NO) production and inhibits smooth muscle cell contraction. This hypothesis was tested in microperfused rabbit renal afferent arterioles, using fluorescence imaging microscopy with the calcium-sensitive dye fura-2 and the NO-sensitive dye 4-amino-5-methylamino-2′,7′-difluorescein. Both dyes were loaded into smooth muscle and endothelium. Depolarization with 100 mmol/l KCl led to a transient vasoconstriction which was converted into a sustained response by N-nitro-l-arginine methyl ester (l-NAME). Depolarization increased smooth muscle cell [Ca2+]ifrom 162 ± 15 nmol/l to a peak of 555 ± 70 nmol/l ( n = 7), and this response was inhibited by 80% by the l-type calcium channel blocker calciseptine. After a delay of 10 s, [Ca2+]iincreased in endothelial cells immediately adjacent to reactive smooth muscle cells, and this calcium wave spread in a nonregenerative fashion laterally into the endothelial cell layer with a velocity of 1.2 μm/s. Depolarization with 100 mmol/l KCl led to a significant increase in NO production ([NO]i) which was inhibited by l-NAME ( n = 5). Acetylcholine caused a rapid increase in endothelial [Ca2+]i, which did not transfer to the smooth muscle cells. l-NAME treatment did not affect changes in smooth muscle [Ca2+]iafter depolarization, but it did increase the calcium sensitivity of the contractile apparatus. We conclude that depolarization increases smooth muscle [Ca2+]iwhich is transferred to the endothelial cells and stimulates NO production which curtails vasoconstriction by reducing the calcium sensitivity of the contractile apparatus.

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