Effect of acute experimental colitis on rabbit colonic smooth muscle

1986 ◽  
Vol 251 (4) ◽  
pp. G538-G545 ◽  
Author(s):  
J. D. Cohen ◽  
H. W. Kao ◽  
S. T. Tan ◽  
J. Lechago ◽  
W. J. Snape
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Current Pulse ◽  
Mechanical Response ◽  
Contractile Activity ◽  
Experimental Colitis ◽  
Isometric Tension ◽  
Mucosal Inflammation ◽  
Resting Membrane Potential ◽  
Circular Smooth Muscle

The membrane potential and contractile activity of colonic circular smooth muscle from New Zealand White rabbits were studied after the production of acute experimental colitis. Colitis was induced in the distal colon by rectal infusion of formaldehyde solution, followed by an intravenous bolus of soluble immune complexes. Despite active mucosal inflammation, there are only occasional inflammatory cells in the muscularis. Electrophysiological studies on tissue from control rabbits and rabbits with colitis were performed using double sucrose gap and intracellular microelectrode techniques. The resting membrane potential was lower (-44 +/- 3 mV) in muscle from rabbits with colitis compared with control animals (-54 +/- 2 mV) (P less than 0.02). Amplitude of the electrotonic potential after a hyperpolarizing current pulse was decreased (P less than 0.05) and the time constant was shortened (P less than 0.01) in muscle from animals with colitis compared with normal animals. Amplitude (13.1 +/- 2.3 mV) and maximum rate of rise (0.24 +/- 0.06 V/s) of the spike potential, initiated by a depolarizing current pulse, were decreased in muscle from animals with colitis compared with muscle from healthy animals (P less than 0.001). Isometric tension generation after electrical and chemical depolarization of the membrane or bethanechol administration was decreased (P less than 0.001) in muscle from colitic animals. These studies suggest 1) membrane resistance and membrane potential are decreased in muscle strips from animals with colitis; and 2) there is a disturbance in the electrical and mechanical response of these tissues after stimulation.

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.

Effect of cold temperature on membrane potential responses in opossum esophageal circular muscle

1989 ◽  
Vol 257 (4) ◽  
pp. G637-G643
Author(s):  
D. Kauvar ◽  
J. Crist ◽  
R. K. Goyal
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Cold Temperature ◽  
Resting Membrane Potential ◽  
Spike Potential ◽  
Circular Smooth Muscle ◽  
Time To Peak ◽  
Proximal Site

The effects of cold temperature on resting membrane potential (RMP) and membrane potential responses to depolarizing electrical current and intramural nerve stimulation were examined in opossum esophageal circular smooth muscle. Intracellular recordings were made in smooth muscle strips obtained from 7 to 8 cm (proximal site) and 1 to 2 cm (distal site) above the lower esophageal sphincter. RMP was not affected by changes in temperature between 34 and 22 degrees C. Cooling caused progressive inhibition of the amplitude and a slight increase in the duration of the spike potential produced by depolarizing current. Cooling did not modify the threshold for spike potential generation but decreased the spike amplitude from 34.0 +/- 0.5 mV at 34 degrees C to 14.1 +/- 2.2 mV at 22 degrees C (P less than 0.01). Electrical field stimulation with single electrical pulses (1.0 ms) produced tetrodotoxin-sensitive biphasic membrane responses consisting of initial hyperpolarization, or an inhibitory junction potential followed by depolarization that increased in amplitude as temperature was decreased from 34 to 26 degrees C and then decreased in amplitude as temperature was further decreased. At both proximal and distal sites cooling from 34 to 22 degrees C caused more than a twofold increase in the duration of hyperpolarization and time to peak depolarization. However, the increase in the absolute time of the duration of hyperpolarization and the time to peak depolarization was significantly greater at the distal than proximal esophageal site. Cooling to 16 degrees C decreased RMP and nearly abolished the biphasic membrane potential response.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of external ions on 45Ca efflux from cat intestinal muscle

1980 ◽  
Vol 238 (6) ◽  
pp. G520-G525
Author(s):  
B. A. Curtis ◽  
D. Kreulen ◽  
C. L. Prosser
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Electrical Stimulation ◽  
Membrane Potential ◽  
Ethylene Glycol ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Tetraacetic Acid ◽  
Circular Smooth Muscle ◽  
45Ca Efflux

The surface-bound Ca of isolated circular smooth muscle of cat small intestine can be removed by substitution of LiCl for NaCl in Krebs solution. This substitution removed surface-bound Ca (45Ca) and allowed us to study transmembrane 45Ca efflux. Neither the resting membrane potential nor contractility changed when Li was substituted for Na. Li removed the same extracellular 45Ca store as did ethylene glycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid. The resting transmembrane 45Ca efflux was inhibited by La3+ and was unchanged in Li, tris(hydroxymethyl)aminomethane, arginine, and sucrose Krebs solution. The extra 45Ca efflux observed upon electrical stimulation was no greater in Na-Krebs than Li-Krebs, but during response to acetylcholine the extra 45Ca efflux was greater in Na-Krebs than Li-Krebs. We conclude that the surface-bound Ca is sensitive to external Na and that the transmembrane Ca efflux is not completely dependent on external Na.

An abnormal rate of actin myosin cross-bridge cycling in colonic smooth muscle associated with experimental colitis

1992 ◽  
Vol 262 (5) ◽  
pp. G921-G926 ◽  
Author(s):  
Y. N. Xie ◽  
W. T. Gerthoffer ◽  
S. N. Reddy ◽  
F. Cominelli ◽  
V. E. Eysselein ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Maximum Velocity ◽  
Experimental Colitis ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Mucosal Inflammation ◽  
Control Group ◽  
Tension Development ◽  
Abnormal Rate ◽  
Mlc Phosphorylation

Previous studies showed that colonic smooth muscle develops less contractile force to neurohumoral stimulation when associated with mucosal inflammation. This study evaluated 1) the Ca2+ dependence for colonic smooth muscle contraction, 2) the maximum velocity of muscle shortening (Vmax), and 3) changes in 20-kDa myosin light-chain (MLC) phosphorylation in distal circular colonic muscle from healthy rabbits and from rabbits with experimental colitis, induced by Formalin and immune complexes. The isometric tension of unskinned muscle stimulated with bethanechol or KCl was less (P less than 0.05) in animals with colitis compared with the control group. In saponin-skinned muscle, the amplitude of the maximal tension at [Ca2+] of 3 x 10(-7) M was decreased (P less than 0.05) in colitis animals (4.3 +/- 0.9 x 10(4) N/m2, n = 7) compared with healthy animals (10.5 +/- 2.4 x 10(4) N/m2, n = 6). However, the ED50 for Ca2+ stimulation was similar (P greater than 0.05) in both groups. When MLC was thiophosphorylated with ATP gamma S, the tension development was decreased in colitis (2.1 +/- 0.3 x 10(4) N/m2, n = 5; P less than 0.01) compared with normals (5.0 +/- 1.4 x 10(4) N/m2, n = 5). In healthy animals, phosphorylation of 20-kDa MLC increased rapidly to 51.2 +/- 3.1% within 15 s after stimulation and subsequently declined to 19.0 +/- 2.1% at 5 min. Vmax was maximal (0.14 Lo/s) 13 s after stimulation and declined before maximal active isometric stress. In colitis animals, the 20-kDa MLC phosphorylation (P less than 0.05) and the Vmax (P less than 0.01) were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for altered circular smooth muscle cell function in lower esophageal sphincter ofW/Wvmutant mice

2011 ◽  
Vol 301 (6) ◽  
pp. G1059-G1065 ◽  
Author(s):  
Francisco Bautista-Cruz ◽  
William G. Paterson
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Lower Esophageal Sphincter ◽  
Mutant Mice ◽  
Resting Membrane Potential ◽  
Circular Smooth Muscle ◽  
Significant Difference ◽  
Esophageal Sphincter ◽  
And Control ◽  
In Cells

Nitrergic neurotransmission to gut smooth muscle is impaired in W/Wvmutant mice, which lack intramuscular interstitial cells of Cajal (ICC-IM). In addition, these mice have been reported to have smaller amplitude unitary potentials (UPs) and a more negative resting membrane potential (RMP) than control mice. These abnormalities have been attributed to absence of ICC-IM, but it remains possible that they are due to alterations at the level of the smooth muscle itself. Amphotericin-B-perforated patch-clamp recordings and Ca2+imaging (fura 2) were compared between freshly isolated single circular smooth muscle cells (CSM) from W/Wvmutant and control mice lower esophageal sphincter (LES). There was no significant difference in seal resistance, capacitance, or input resistance in response to applied electrotonic current pulses between CSM cells from W/Wvmutants and controls. Compared with control mice, RMP was more negative and UPs significantly smaller in CSM cells from mutant mice LES. Administration of caffeine induced an inward current in cells from both mutant and control mice, but the current density was significantly larger in cells from W/Wvmutants. Membrane potential hyperpolarization induced by sodium nitroprusside was larger in cells from control mice vs. W/Wvmutants. In addition, intracellular Ca2+transients induced by caffeine were significantly increased in cells from mutants. These findings indicate that LES CSM is abnormal in W/Wvmutant mice. Thus some physiological functions attributed to ICC-IM based on experiments in smooth muscle of ICC deficient mice may need to be reconsidered.

Molecular and functional characterization of ERG, KCNQ, and KCNE subtypes in rat stomach smooth muscle

2002 ◽  
Vol 282 (2) ◽  
pp. G277-G287 ◽  
Author(s):  
Susumu Ohya ◽  
Keiichi Asakura ◽  
Katsuhiko Muraki ◽  
Minoru Watanabe ◽  
Yuji Imaizumi
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Functional Characterization ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Rt Pcr ◽  
Rat Stomach ◽  
Circular Smooth Muscle ◽  
Stomach Fundus

Contribution of K+ channels derived from the expression of ERG, KCNQ, and KCNE subtypes, which are responsible for rapidly and slowly activating delayed rectifier K+ currents ( I Kr and I Ks, respectively) in cardiac myocytes, to membrane currents was examined in stomach circular smooth muscle cells (SMCs). The region-qualified multicell RT-PCR showed that ERG1/KCNE2 transcripts were expressed in rat stomach fundus and antrum SMCs and that KCNQ1/KCNE1 transcripts were expressed in antrum but not fundus. Western blotting and immunocytochemical analyses indicate that ERG1 proteins were substantially expressed in both regions, whereas KCNE1 proteins were faintly expressed in antrum and not in fundus. Both I Kr- and I Ks-like currents susceptible to E-4031 and indapamide, respectively, were identified in circular SMCs of antrum but only I Kr-like current was identified in fundus. It is strongly suggested that I Kr- and I Ks-like currents functionally identified in rat stomach SMCs are attributable to the expression of ERG1/KCNE2 and KCNQ1/KCNE1, respectively. The membrane depolarization by 1 μM E-4031 indicates the contribution of K+ channels encoded by ERG1/KCNE2 to the resting membrane potential in stomach SMCs.

Neural and myogenic effects of cyclooxygenase products on canine bronchial smooth muscle

1995 ◽  
Vol 268 (1) ◽  
pp. L47-L55 ◽  
Author(s):  
A. P. Abela ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Field Stimulation ◽  
Resting Membrane Potential ◽  
Dependent Manner ◽  
Ach Release ◽  
Concentration Dependent Manner ◽  
Excitatory Junction Potentials ◽  
Pg E2 ◽  
Large Contraction

In canine bronchi bathed in 10(-6) M indomethacin (IDM), prostaglandin (PG) E2 inhibited electrical field stimulation (EFS)- and acetylcholine (ACh)-mediated contractions and excitatory junction potentials (EJP) in a concentration-dependent manner without altering the resting membrane potential. EFS-induced EJPs were abolished at 10(-7) M PGE2, which shifted responses to ACh 10-fold rightward. Thus PGE2 predominantly inhibited the release of ACh and secondarily decreased smooth muscle response to ACh. U-46619, an analogue of thromboxane A2 (TxA2), initiated tetrodotoxin- and atropine-insensitive contractions in a concentration-dependent manner. U-46619 (10(-9) M) did not alter significantly EFS- or ACh-stimulated contractions and potentiated EFS amplitude of EJPs without depolarizing muscle cells. Either prejunctional activation of ACh release by TxA2 or postjunctional potentiation of the response to ACh can explain these findings. U-46619 (<or = 10(-8) M) depolarized the membrane potential, initiating oscillations accompanied by a large contraction. Addition of 10(-8) M nitrendipine, but not tetraethylammonium (25 mM), blocked the oscillations selectively. Other prostanoids (PGD2, PGI2, and PGF2 alpha) had no significant effects on canine bronchi. In the absence of IDM, PGE2 accumulated, EFS contractions decreased with time, and EJPs disappeared. We conclude that in canine bronchi PGE2 predominantly inhibits ACh release and endogenous PGE2 acts similarly, whereas TxA2 excites, probably at postjunctional sites.

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat

1987 ◽  
Vol 252 (5) ◽  
pp. G654-G661
Author(s):  
W. J. Snape ◽  
S. T. Tan ◽  
H. W. Kao
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Spike Activity ◽  
Membrane Resistance ◽  
Wave Pattern ◽  
Isometric Tension ◽  
Muscle Membrane ◽  
Maximum Effect ◽  
Smooth Muscle Membrane

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

scholarly journals Effects of endothelin-1 on the membrane potential and slow waves in circular smooth muscle of rat gastric antrum

2004 ◽  
Vol 40 (4/5) ◽  
pp. 199-210 ◽  
Author(s):  
Kenro Imaeda ◽  
Takashi Kato ◽  
Naotsuka Okayama ◽  
Seiji Imai ◽  
Makoto Sasaki ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Gastric Antrum ◽  
Slow Waves ◽  
Endothelin 1 ◽  
Circular Smooth Muscle

In vivo membrane potentials of smooth muscle cells in the caudal artery of the rat

1985 ◽  
Vol 249 (1) ◽  
pp. C78-C83 ◽  
Author(s):  
H. J. Bryant ◽  
D. R. Harder ◽  
M. B. Pamnani ◽  
F. J. Haddy
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Humoral Factors ◽  
Caudal Artery ◽  
Blood Pressures

Membrane potentials measured in vivo may differ significantly from those measured in vitro in part due to humoral factors, innervation, and wall tension. These studies were initiated to determine whether it is feasible to record membrane potentials from vascular smooth muscle cells in vivo in the caudal artery of the pentobarbital-anesthetized male Wistar rat. Membrane potentials were measured using glass microelectrodes and correlated with systolic, diastolic, and mean blood pressures. For systolic blood pressures between 100 and 140 mmHg the average resting membrane potential was -38.4 +/- 0.48 mV. There was good correlation of systolic, diastolic, and mean blood pressures with membrane potential between 100 and 140 mmHg (r = 0.89, 0.75, and 0.89, respectively). Below 80 mmHg the arterial muscle cells became more depolarized than would be expected if the membrane potential were determined solely by transmural pressure. The depolarized membrane potential at low arterial pressures may be due to enhanced neural input. Spontaneous electrical activity was observed in some of the in vivo cells. When action potentials were present, they were generated at rates between 1-2/s and 6-7/min. These studies indicate that it is feasible to measure membrane potentials from arterial smooth muscle cells in vivo in the caudal artery of the rat.

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