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.

scholarly journals Inward current in single smooth muscle cells of the guinea pig taenia coli.

1989 ◽  
Vol 93 (3) ◽  
pp. 521-550 ◽  
Author(s):  
Y Yamamoto ◽  
S L Hu ◽  
C Y Kao
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Reversal Potential ◽  
Muscle Cells ◽  
Taenia Coli ◽  
Average Cell ◽  
Time Constants ◽  
Inward Current

Using the tight-seal voltage-clamp method, the ionic currents in the enzymatically dispersed single smooth muscle cells of the guinea pig taenia coli have been studied. In a physiological medium containing 3 mM Ca2+, the cells are gently tapering spindles, averaging 201 (length) x 8 microns (largest diameter in center of cell), with a volume of 5 pl. The average cell capacitance is 50 pF, and the specific membrane capacitance 1.15 microF/cm2. The input impedance of the resting cell is 1-2 G omega. Spatially uniform voltage-control prevails after the first 400 microseconds. There is much overlap of the inward and outward currents, but the inward current can be isolated by applying Cs+ internally to block all potassium currents. The inward current is carried by Ca2+. Activation begins at approximately -30 mV, maximum ICa occurs at +10-+20 mV, and the reversal potential is approximately +75 mV. The Ca2+ channel is permeable to Sr2+ and Ba2+, and to Cs+ moving outwards, but not to Na+ moving inwards. Activation and deactivation are very rapid at approximately 33 degrees C, with time-constants of less than 1 ms. Inactivation has a complex time course, resolvable into three exponential components, with average time constants (at 0 mV) of 7, 45, and 400 ms, which are affected differently by voltage. Steady-state inactivation is half-maximal at -30 mV for all components combined, but -36 mV for the fast component and -26 and -23 mV for the other two components. The presence of multiple forms of Ca2+ channel is inferred from the inactivation characteristics, not from activation properties. Recovery of the fast channel occurs with a time-constant of 72 ms (at +10 mV). Ca2+ influx during an action potential can transfer approximately 9 pC of charge, which could elevate intracellular Ca2+ concentration adequately for various physiological functions.

scholarly journals Calcium Channels and Nifedipine Inhibition of Serotonin-Induced [3H]Thymidine Incorporation in Cultured Cerebral Smooth Muscle Cells

1992 ◽  
Vol 12 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Thomas A. Kent ◽  
Allahyar Jazayeri ◽  
J. Marc Simard
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Thymidine Incorporation ◽  
Membrane Surface ◽  
Muscle Cells ◽  
Thymidine Uptake ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Alternate Mechanism

Cultures of smooth muscle cells were prepared from the basilar artery of adult guinea pigs. Passaged cultures (10–30 passages) that expressed serotonin receptors were studied using [3H]thymidine incorporation. When tested in quiescent medium, serotonin potently stimulated [3H]thymidine incorporation (EC50 of 31 n M) by as much as 400% at 24 h. The number of cells was not significantly increased at 24 or 48 h. At concentrations of 10−8–10−5 M 5-HT, [3H]thymidine uptake was reduced 40–50% by the dihydropyridine Ca2+ channel blocker, nifedipine (1 μ M). To demonstrate a possible mechanism for the sensitivity to nifedipine, Ca2+ currents were measured using the whole cell patch clamp technique. The cells expressed dihydropyridine-sensitive L-type Ca2+ channels, but not other subtypes of Ca2+ channels, as indicated by the kinetic and voltage-dependent characteristics of the current and by the stimulatory effect of Bay K 8644. The magnitude of the Ca2+ currents was related exponentially to the membrane surface area, measured as cell capacitance. These data support the association of dihydropyridine-sensitive Ca2+ channels with mitogenesis in vascular smooth muscle, and suggest an alternate mechanism of action for the beneficial effect of dihydropyridines in prophylaxis of cerebral vasospasm.

ω-3 Polyunsaturated fatty acids—modulation of voltage-dependent L-type Ca2+ current in guinea-pig tracheal smooth muscle cells

1998 ◽  
Vol 355 (2-3) ◽  
pp. 257-266 ◽  
Author(s):  
Hisanori Hazama ◽  
Toshiaki Nakajima ◽  
Michiko Asano ◽  
Kuniaki Iwasawa ◽  
Toshihiro Morita ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Guinea Pig ◽  
Polyunsaturated Fatty Acids ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tracheal Smooth Muscle ◽  
Voltage Dependent

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.

Preferential potentiation by hypotonic cell swelling of muscarinic cation current in guinea pig ileum

1997 ◽  
Vol 272 (1) ◽  
pp. C240-C253 ◽  
Author(s):  
Y. Waniishi ◽  
R. Inoue ◽  
Y. Ito
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscarinic Receptor ◽  
Time Course ◽  
Cell Swelling ◽  
Patch Clamp Technique ◽  
Cationic Current ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Hypotonic Cell Swelling

The effects of hypotonic cell swelling (HCS) on muscarinic receptor-activated cationic current in guinea pig ileal smooth muscle were investigated by the whole cell patch-clamp technique. With nystatin-perforated recording, reduced external tonicity from 312 to 262 mosM caused cell swelling but hardly affected the membrane currents activated by depolarization, such as outward-rectifying K and voltage-dependent Ca currents. In contrast, the inward current evoked by carbachol at -60 mV was greatly increased (approximately 50%) by the same extent of hypotonicity. This effect is likely to occur through potentiation of nonselective cation channels coupled to the muscarinic receptor (mNSCCs) and probably does not involve elevated intracellular Ca2+ concentration ([Ca2+]i), since neither removal of external Ca2+ nor [Ca2+]i buffering with 10 mM 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid significantly affected the results. Furthermore, the time course and degree of this potentiation closely matched those of video-microscopically monitored HCS. These results support the view that mechanosensitive modulation may be a powerful mechanism to regulate mNSCCs activity in gut smooth muscle, together with membrane potential and [Ca2+]i.

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

Nitric oxide suppresses a Ca2+-stimulated Cl− current in smooth muscle cells of opossum esophagus

1998 ◽  
Vol 274 (5) ◽  
pp. G886-G890 ◽  
Author(s):  
Yong Zhang ◽  
Fivos Vogalis ◽  
Raj K. Goyal
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscles ◽  
Reversal Potential ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Patch Clamp Technique ◽  
No Donor ◽  
Pipette Solution

Nitric oxide (NO) hyperpolarizes visceral smooth muscles. Using the patch-clamp technique, we investigated the possibility that NO-mediated hyperpolarization in the circular muscle of opossum esophagus results from the suppression of a Ca2+-stimulated Cl− current. Smooth muscle cells were dissociated from the circular layer and bathed in high-K+Ca2+-EGTA-buffered solution. Macroscopic ramp currents were recorded from cell-attached patches. Contaminating K+-channel currents were blocked with tetrapentylammonium chloride (200 μM) added to all solutions. Raising bath Ca2+concentration above 150 nM in the presence of A-23187 (10 μM) activated a leak current ( I L-Ca) with an EC50 of 1.2 μM at −100 mV. The reversal potential ( E rev) of I L-Ca (−8.5 ± 1.8 mV, n = 8) was significantly different ( P < 0.05) from E rev of the background current (+4.2 ± 1.2 mV, n = 8). Equimolar substitution of 135 mM Cl− in the pipette solution with gluconate significantly shifted E rev of I L-Ca to +16.6 ± 3.4 mV ( n = 4) ( P < 0.05 compared with background), whereas replacement of total Na+with Tris+ suppressed I L-Ca but did not affect E rev(−15 ± 3 mV, n = 3; P > 0.05). I L-Ca was inhibited by DIDS (500 μM). Diethylenetriamine-NO adduct (200 μM), a NO• donor, and 8-bromo-cGMP (200 μM) suppressed I L-Ca by 59 ± 15% ( n = 5) and 62 ± 21% ( n = 4) at −100 mV, respectively. We conclude that in opossum esophageal smooth muscle NO-mediated hyperpolarization may be produced by suppression of a Ca2+-stimulated Cl−-permeable conductance via formation of cGMP.

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