scholarly journals Depolarization-Stimulated Contractility of Gastrointestinal Smooth Muscle in Calcium-Free Solution: A Review

2011 ◽  
Vol 2011 ◽  
pp. 1-3 ◽  
Author(s):  
Emily D. Evans ◽  
Allen W. Mangel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Threshold Level ◽  
Slow Waves ◽  
Free Solution ◽  
Gastrointestinal Smooth Muscle ◽  
Small Muscle

The membrane of most gastrointestinal smooth muscles shows slow waves, slow rhythmic changes in membrane potential. Slow waves serve to bring the membrane potential of smooth muscle cells to a threshold level that elicits a second electrical event known as the spike or action potential. The inward current of the spike, in most gastrointestinal smooth muscle preparations, is carried, at least in part, by calcium. Indeed, considering the narrow diameter of smooth muscle cells, some have hypothesized that the influx of calcium during the spike is sufficient for activation of the contractile machinery. Findings consistent with this include marked reduction in contractility during exposure of muscle segments to blockers of L-type calcium channels or following reductions in external calcium levels. However, it has also been observed that following exposure of muscle segments to external bathing solutions containing no added calcium plus 5 mM EGTA to remove any remaining extracellular calcium, contractions can be triggered following membrane depolarization. It is noteworthy that in isolated smooth muscle cells or in small muscle segments, during incubation in calcium-free solution, depolarization does not induce contractions. The present paper discusses the evidence in support of depolarization-mediated contractions occurring in gastrointestinal smooth muscle segments during incubation in solutions devoid of calcium.

scholarly journals Membrane potential of smooth muscle cells in K-free solution

1971 ◽  
Vol 217 (2) ◽  
pp. 281-295 ◽  
Author(s):  
R. Casteels ◽  
G. Droogmans ◽  
H. Hendrickx
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Free Solution

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.

Endothelial and smooth muscle cells hyperpolarized by bradykinin are not dye coupled

1990 ◽  
Vol 258 (3) ◽  
pp. H836-H841 ◽  
Author(s):  
J. L. Beny
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Lucifer Yellow ◽  
Electrical Response ◽  
Electrical Coupling ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Electrical Signal

The membrane potential of endothelial and neighboring (0.1 mm) smooth muscle cells of pig coronary arteries were simultaneously recorded with two microelectrodes. The membrane potential of endothelial cells was -40 +/- 4 mV (n = 9). In these cells bradykinin (250 nM), an endothelium-dependent vasodilator, evoked a transient hyperpolarization (14 +/- 2 mV, n = 9) resembling those already observed in smooth muscles. The similarity between the electrical signal of pre- and postmyoendothelial junctions suggested an electrical coupling between endothelial and smooth muscle cells. However, the injection of the fluorescent dye Lucifer yellow in the recorded cell proved that the cell was endothelial, and in addition, the injection demonstrated the absence of dye coupling between endothelial and smooth muscle cells. Moreover the injection of electrical pulses (0.05-3.5 nA) in the endothelial cell never evoked any electrical response in the smooth muscle. By contrast, the smooth muscle cells were electrically coupled-together. These results do not support the idea that the endothelial cell hyperpolarization caused by bradykinin is transmitted to smooth muscle cells by electrotonic spreading.

Electrical properties of smooth muscle cell membrane in renal pelvis of rabbits

1990 ◽  
Vol 259 (6) ◽  
pp. F888-F894 ◽  
Author(s):  
N. Seki ◽  
H. Suzuki
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Slow Wave ◽  
Renal Pelvis ◽  
Smooth Muscles ◽  
Marked Change ◽  
Muscle Cells ◽  
Slow Waves ◽  
Maximum Slope

Intracellular recordings were made to study the electrical properties of smooth muscle cells in the rabbit renal pelvis. The muscle cells exhibited spontaneous oscillation in the membrane potential (slow wave). The slow waves were regular and were resistant to tetrodotoxin and sympathomimetic or parasympathomimetic antagonists, findings indicative of myogenic activity. The membrane was depolarized by an increase in extracellular concentration of K+ ([K+]o), decrease in [Na+]o, inhibition of the electrogenic Na(+)-K+ pump by ouabain or K(+)-free solution, and the application of norepinephrine (NE, greater than 10(-6) M). The maximum slope of the membrane depolarization produced by a 10-fold increase in [K+]o was approximately 48 mV. Reductions in [Ca2+]o inhibited the generation of slow waves with no marked change in the membrane potential. Depolarizations produced by any given method increased the frequency and decreased the amplitude of the slow wave, and NE had the most potent accelerating action on the frequency. Hyperpolarization of the membrane by 1-5 mV with extracellularly applied current stimuli reduced the frequency, and a strong hyperpolarization (greater than 5 mV) blocked the generation of slow waves. Electrophysiological properties of the slow waves obtained with tissues of the renal pelvis and intestinal smooth muscles were compared.

scholarly journals TRPC6 regulates phenotypic switching of vascular smooth muscle cells through plasma membrane potential‐dependent coupling with PTEN

2019 ◽  
Vol 33 (9) ◽  
pp. 9785-9796 ◽  
Author(s):  
Takuro Numaga‐Tomita ◽  
Tsukasa Shimauchi ◽  
Sayaka Oda ◽  
Tomohiro Tanaka ◽  
Kazuhiro Nishiyama ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Phenotypic Switching ◽  
Plasma Membrane Potential

Beta-adrenergic actions on membrane electrical properties of dissociated smooth muscle cells

1988 ◽  
Vol 254 (3) ◽  
pp. C423-C431 ◽  
Author(s):  
H. Yamaguchi ◽  
T. W. Honeyman ◽  
F. S. Fay
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Beta Adrenergic

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals TGF-β suppresses the upregulation of MMP-2 by vascular smooth muscle cells in response to PDGF-BB

2010 ◽  
Vol 298 (1) ◽  
pp. C191-C201 ◽  
Author(s):  
George M. Risinger ◽  
Dawn L. Updike ◽  
Elizabeth C. Bullen ◽  
James J. Tomasek ◽  
Eric W. Howard
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Transforming Growth Factor ◽  
Focal Adhesions ◽  
Muscle Cells ◽  
Threshold Level ◽  
Inhibitory Signaling

During platelet-derived growth factor (PDGF)-BB-mediated recruitment to neovascular sprouts, vascular smooth muscle cells (VSMCs) dedifferentiate from a contractile to a migratory phenotype. This involves the downregulation of contractile markers such as smooth muscle (SM) α-actin and the upregulation of promigration genes such as matrix metalloproteinase (MMP)-2. The regulation of MMP-2 in response to PDGF-BB is complex and involves both stimulatory and inhibitory signaling pathways, resulting in a significant delay in upregulation. Here, we provide evidence that the delay in MMP-2 upregulation may be due to the autocrine expression and activation of transforming growth factor (TGF)-β, which is known to promote the contractile phenotype in VSMCs. Whereas PDGF-BB could induce the loss of stress fibers and focal adhesions, TGF-β was able to block or reverse this transition to a noncontractile state. TGF-β did not, however, suppress early signaling events stimulated by PDGF-BB. Over time, though PDGF-BB induced increased TGF-β1 levels, it suppressed TGF-β2 and TGF-β3 expression, leading to a net decrease in the total TGF-β pool, resulting in the upregulation of MMP-2. Together, these findings indicate that MMP-2 expression is suppressed by a threshold level of active TGF-β, which in turn promotes a contractile VSMC phenotype that prevents the upregulation of MMP-2.

Role of HERG-like K+ currents in opossum esophageal circular smooth muscle

1999 ◽  
Vol 277 (6) ◽  
pp. C1284-C1290 ◽  
Author(s):  
Hamid I. Akbarali ◽  
Hemant Thatte ◽  
Xue Dao He ◽  
Wayne R. Giles ◽  
Raj K. Goyal
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Single Cells ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
Circular Smooth Muscle ◽  
Inward Currents

An inwardly rectifying K+ conductance closely resembling the human ether-a-go-go-related gene (HERG) current was identified in single smooth muscle cells of opossum esophageal circular muscle. When cells were voltage clamped at 0 mV, in isotonic K+ solution (140 mM), step hyperpolarizations to −120 mV in 10-mV increments resulted in large inward currents that activated rapidly and then declined slowly (inactivated) during the test pulse in a time- and voltage- dependent fashion. The HERG K+ channel blockers E-4031 (1 μM), cisapride (1 μM), and La3+ (100 μM) strongly inhibited these currents as did millimolar concentrations of Ba2+. Immunoflourescence staining with anti-HERG antibody in single cells resulted in punctate staining at the sarcolemma. At membrane potentials near the resting membrane potential (−50 to −70 mV), this K+ conductance did not inactivate completely. In conventional microelectrode recordings, both E-4031 and cisapride depolarized tissue strips by 10 mV and also induced phasic contractions. In combination, these results provide direct experimental evidence for expression of HERG-like K+ currents in gastrointestinal smooth muscle cells and suggest that HERG plays an important role in modulating the resting membrane potential.

Isolation of smooth muscle cells from swine carotid artery by digestion with papain

1986 ◽  
Vol 251 (3) ◽  
pp. C474-C481 ◽  
Author(s):  
S. P. Driska ◽  
R. Porter
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Smooth Muscle Cells ◽  
Single Cells ◽  
Calcium Ionophore ◽  
Muscle Cells ◽  
Ionophore A23187 ◽  
Free Solution ◽  
Isolated Cells ◽  
Viable Cells

A new method is described for the preparation of viable, elongated smooth muscle cells from the swine carotid artery. Cells were prepared by papain digestion of pressurized arteries in calcium-free solution. After digestion, the arteries were everted, and fine strips were teased from the intimal surface of the media in calcium-free solution, releasing single cells. Viability was assessed by exclusion of trypan blue and by appearance under phase-contrast microscopy. By these criteria, approximately 20% of the isolated cells were viable. The most distinguishing and unexpected characteristic of these cells was their length. Mean length of the relaxed viable cells was 240.4 +/- 47.4 microns (SD, n = 76), which is much longer than previously reported for arterial smooth muscle cells. Calcium (1.6 mM) caused most of the viable cells to contract slightly, and the mean cell length in calcium was 194.4 +/- 57.7 microns. Cells in 1.6 mM calcium contracted substantially in response to 10 microM histamine or the calcium ionophore A23187 (10 microM), demonstrating that histamine receptors and the contractile apparatus were still functional.

Characterization of [3H]nifedipine binding to intact vascular smooth muscle cells

1988 ◽  
Vol 254 (1) ◽  
pp. C45-C52 ◽  
Author(s):  
K. Sumimoto ◽  
M. Hirata ◽  
H. Kuriyama
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Binding Capacity ◽  
Specific Binding ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Scatchard Analysis ◽  
Intact Cells ◽  
Porcine Coronary Artery ◽  
Control Value

Specific binding of the dihydropyridine Ca2+ antagonist [3H]nifedipine to dispersed smooth muscle cells of the porcine coronary artery was investigated and the findings were compared with the binding to microsomes of smooth muscles. Specific binding to intact cells was saturable and reversible. The dissociation constant was 1.93 +/- 0.42 nM and the maximal binding capacity was 59.6 +/- 12.4 fmol/10(6) cells, as assessed by Scatchard analysis of the equilibrium binding at 25 degrees C. The Kd value with intact cells was slightly higher than that observed with microsomes. Specific binding of [3H]nifedipine to intact cells was completely displaced by unlabeled dihydropyridine derivatives. Among other Ca2+ antagonists, verapamil and d-cis-diltiazem partially and flunarizine completely inhibited the binding. In the case of microsomes, d-cis-diltiazem stimulated the binding of [3H]nifedipine. These results suggest that there may be multiple binding sites for different subclasses of Ca2+ antagonists. Polyvalent cations had no effect on the binding to intact cells. In the case of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA)-treated microsomes, the addition of CaCl2 and BaCl2 increased the Bmax, but the Kd value remained unchanged. MnCl2 and CdCl2 had stimulatory or inhibitory effects, depending on the concentrations, whereas LaCl3 had no effect. The effect of membrane depolarization on the binding was also examined. When the intact cells were incubated in high [K+]o solution for 60 min, the Kd was lowered to 1.4 nM from the control value of 2.0 nM, thereby indicating that [3H]nifedipine binds to Ca2+ channels, with a higher affinity, at depolarized states.

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