Initiation of distension-induced descending peristaltic reflex in opossum esophagus: role of muscle contractility

2001 ◽  
Vol 280 (3) ◽  
pp. G431-G438 ◽  
Author(s):  
A. Muinuddin ◽  
W. G. Paterson
Keyword(s):  
Smooth Muscle ◽  
Muscle Tension ◽  
Organ Bath ◽  
Dependent Manner ◽  
Krebs Solution ◽  
Muscle Contractility ◽  
Concentration Dependent Manner ◽  
Peristaltic Reflex ◽  
Over The Top

The balloon distension (BD)-induced descending peristaltic reflex in the opossum smooth muscle esophagus is abolished in vitro when a Ca2+-free Krebs solution is placed at the site of distension, suggesting that either synaptic transmission occurs at the origin of the reflex or initiation of the reflex requires the development of muscle tension in response to BD. To test the latter possibility, an 8- to 10-cm length of smooth muscle esophagus was placed in a dual-chamber organ bath, isolating the stimulating (orad) from the recording site (aborad). Nifedipine addition to the orad chamber (i.e., site of distension) inhibited the BD-induced “off” contractions in both chambers in a concentration-dependent manner. However, the aborad response to electrical field stimulation (EFS) was unaffected. Atropine addition to the orad chamber had no effect on BD or EFS responses in either chamber. To examine the effects of these agents on tonic contractility, an isobaric barostat was employed. Pressure-volume curves were not altered by Ca2+-free Krebs solution, nifedipine, or TTX, suggesting that resting esophageal tone is not dependent on neural factors or muscle contractility. However, both Ca2+-free Krebs solution and nifedipine markedly decreased phasic contractions over the top of the distending bag. These observations suggest that local, stretch-induced phasic muscle contraction is required for initiation of the BD-induced descending peristaltic reflex.

scholarly journals Bronchodilator effect of apigenin and luteolin, two components of Dracocephalum kotschyi on isolated rabbit trachea

2019 ◽  
Vol 8 (4) ◽  
pp. 281-286 ◽  
Author(s):  
Hassan Sadraei ◽  
Seyed Mostapha Ghanadian ◽  
Gholamreza Asghari ◽  
Aminreza Gavahian
Keyword(s):  
Smooth Muscle ◽  
Tracheal Ring ◽  
Tracheal Smooth Muscle ◽  
Organ Bath ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Standard Drug ◽  
Solvent Fractionation ◽  
Dracocephalum Kotschyi

Introduction: Dracocephalum kotschyi is a native Iranian plant with antispasmodic activities on smooth muscles such as ileum and uterus. However, so far antispasmodic effect of D. kotschyi on tracheal smooth muscle has not been reported. Therefore, the objective of this research was to investigate antispasmodic activity of D. kotschyi extract and two of its components luteolin and apigenin on rabbit tracheal contraction in vitro. Methods: Rabbits were euthanized by carbon dioxide and the trachea was dissected and immersed in a Tyrode’s solution. Tracheal rings were prepared and mounted vertically in an organ bath at 37°C and gassed continuously with O2. The tracheal ring preparations were contracted with acetylcholine (ACh) and KCl. The isotonic tension was recorded before and after addition of aminophylline, apigenin, luteolin or flavonoids rich extract of D. kotschyi. Flavonoids rich extract were prepared from D. kotschyi using solvent-solvent fractionation technique. Results: Standard drug aminophylline, prevented tracheal ring preparation contracted with ACh. Cumulative addition of aminophylline also attenuated tonic contraction induced by KCl on tracheal smooth muscle. D. kotschyi extract at concentration ranges of 32-512 μg/mL in a concentration dependent manner inhibited KCl and ACh induced tracheal contraction. Apigenin and luteolin (range 16–512 μg/mL) relaxed KCl and ACh-induced contraction of tracheal smooth muscle in vitro in a concentration-dependent manner. Conclusion: This study demonstrated that D. kotschyi extract is a relaxant of tracheal smooth muscle. The relaxant effect of D. kotschyi extract could be due to its flavonoids component such as apigenin and luteolin.

scholarly journals Role of α1-adrenergic receptor subtypes in contractility of the rabbit abdominal aorta in vitro

2013 ◽  
Vol 82 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Jan Gnus ◽  
Albert Czerski ◽  
Stanisław Ferenc ◽  
Wojciech Zawadzki ◽  
Wojciech Witkiewicz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Receptor Antagonist ◽  
Abdominal Aorta ◽  
Adrenergic Receptor ◽  
Receptor Subtypes ◽  
Organ Bath ◽  
Dependent Manner ◽  
Receptor Antagonists ◽  
Selective Antagonists

Investigation of the effect of α1-adrenergic receptor subtypes on the contraction of the abdominal aorta will allow for more effective treatment of hypertension by use of selective antagonists. The aim of the study was to evaluate the participation of α1-adrenergic receptor subtypes in the contractility of the aortic smooth muscle cells in rabbits. The in vitro experiments were performed in isolated tissue preparations from 30 adult female New Zealand rabbits. The abdominal aortic sections were placed in organ bath chambers and contracted with increasing doses of non-selective α1-adrenergic receptor agonist phenylephrine without pre-incubation or after incubation in α1-adrenergic receptor subtype-selective or non-selective antagonists. Separate sections were incubated with increasing concentrations of antagonists. Phenylephrine caused maximal rise in arterial smooth muscle tone to 4.75 ± 0.47 mN. The most potent in blocking phenylephrine induced contraction was 5-metylurapidil (α1A-adrenergic receptor antagonist) followed by phentolamine and prazosin (non-selective α1-adrenergic receptor antagonists); BMY 7378 (α1D-adrenergic receptor antagonist), cyclazosin and L-765.314 (α1B-adrenergic receptor antagonists) were less effective. All antagonists, except BMY 7378 elicited relaxation of non-precontracted aorta in dose dependent manner. Our results indicate that postsynaptic α1A receptors are the most potent in producing rabbit abdominal aorta contraction, while α1B and α1D subtypes are less effective.

scholarly journals Effects of enantiomers of β2-agonists on ACh release and smooth muscle contraction in the trachea

1998 ◽  
Vol 274 (1) ◽  
pp. L32-L38 ◽  
Author(s):  
Xiang-Yang Zhang ◽  
Feng-Xia Zhu ◽  
Michal A. Olszewski ◽  
N. Edward Robinson
Keyword(s):  
Smooth Muscle ◽  
High Performance ◽  
Muscle Tension ◽  
Electrical Field Stimulation ◽  
Smooth Muscle Contraction ◽  
Acute Administration ◽  
Dependent Manner ◽  
Ach Release ◽  
Concentration Dependent Manner ◽  
Parasympathetic Nerves

The β2-agonists currently used as bronchodilators are racemic mixtures of R- and S-enantiomers. In the present study, we examined the effects of enantiomers of the β2-agonists albuterol and formoterol on acetylcholine (ACh) release from equine trachealis parasympathetic nerves. ACh release was evoked by electrical field stimulation (20 V, 0.5 ms, 0.5 Hz) and measured by high-performance liquid chromatography coupled with electrochemical detection. We also tested the effects of enantiomers of albuterol and formoterol on equine tracheal smooth muscle (TSM) contraction in response to exogenous ACh. R- and RS-albuterol (10−8 to 10−5 M) and RR- and RR/SS-formoterol (10−8 to 10−5 M) augmented ACh release in a concentration-dependent manner. Beginning at 10−6 M, SS-formoterol significantly increased ACh release, and at 10−5 M, release increased by 71.9 ± 8.7% over baseline. This effect was only observed, however, when the prejunctional muscarinic autoinhibitory effect of ACh was prevented with atropine. Both the RR- and SS-formoterol-induced increases in ACh release were abolished by the β2-antagonist ICI-118551 (3 × 10−7 M). The effect of S-albuterol on ACh release was variable, and the mean increase induced by 10−5 M was 30.8 ± 16.1% in the presence of atropine. In the muscle tension study, R- and RS-albuterol and RR- and RR/SS-formoterol (10−8 to 10−5 M) but not the S-enantiomers inhibited TSM contraction. Even though R-enantiomers augment ACh release, they potently inhibit TSM contraction. Because racemic β2-agonists are bronchodilators on acute administration, the postjunctional spasmolytic effects of R-enantiomers predominate over the spasmogenic effect evoked via increased ACh release. The S-enantiomers, in contrast, do not inhibit TSM contraction and therefore would not contribute to the observed bronchodilation of the racemate. The S-enantiomers do prejunctionally facilitate ACh release when prejunctional muscarinic autoreceptors are dysfunctional, suggesting a potentially deleterious effect.

scholarly journals Effects of Ursolic Acid on Contractile Activity of Gastric Smooth Muscles

2015 ◽  
Vol 10 (4) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Natalia Prissadova ◽  
Petko Bozov ◽  
Kiril Marinkov ◽  
Hristo Badakov ◽  
Atanas Kristev
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Ursolic Acid ◽  
Slow Wave ◽  
Contractile Activity ◽  
Smooth Muscles ◽  
Dependent Manner ◽  
Krebs Solution ◽  
Concentration Dependent Manner ◽  
Gastric Smooth Muscle

Ursolic acid (UA) in concentrations of 1×10−7 mol/L - 5×10−5 mol/L induced relaxation in gastric smooth muscle (SM) tissues, in a concentration-dependent manner. The relaxation did not change membrane potential and slow wave contraction patterns. A significant decrease in amplitude and frequency of spike-potentials was observed. UA-induced reactivity was removed when SM preparations were treated with nifedipine (1×10−6 mol/L). Ca2+- induced contractions of the depolarized SM preparations (42 mmol/L K+; Ca2+- free Krebs solution) were substantially reduced in the presence of UA. It was determined that, in certain concentrations, UA influenced L – type Ca2+ channels, and reduced the Ca2+ influx.

scholarly journals Phytochemical Evaluation of Lythrum Salicaria Extracts and Their Effects on Guinea-Pig Ileum

2013 ◽  
Vol 8 (9) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Tímea Bencsik ◽  
Loránd Barthó ◽  
Viktor Sándor ◽  
Nóra Papp ◽  
Rita Benkó ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Ethyl Acetate ◽  
Water Extract ◽  
Lythrum Salicaria ◽  
Dependent Manner ◽  
Guinea Pig Ileum ◽  
Concentration Dependent Manner ◽  
Ethanol In Water

n-Hexane, chloroform, ethyl acetate and 50% ethanol in water extracts prepared from the air-dried flowering parts of Lythrum salicaria L. were tested for in vitro pharmacological properties on Guinea-pig ileum, which is suitable for detecting a whole range of neuronal and smooth muscle effects. UHPLC-MS was used to evaluate polyphenol components of the extracts. In the ileum, the most prominent response (46.4% related to 0.5 μM histamine) of the extracts causing smooth muscle contractions were triggered by the 50% ethanol in water extract in a concentration-dependent manner. Atropine, indomethacin and PPADS plus suramin significantly reduced the contractile response caused by this extract. The strongest inhibition was due to atropine. The results suggest that L. salicaria extracts have a moderate muscarinic receptor agonist effect in Guinea-pig ileum and that prostanoids and purinoceptor mechanisms are involved to some extent. Therefore diluted extracts of L. salicaria p.o. could be used as a mild stimulant of gastrointestinal motility. The 50% ethanol in water extract was rich in polyphenols. n-Hexane, chloroform and ethyl acetate extracts failed to contain catechin, caffeic acid, quercetin-3-D-galactoside and rutin, but they all showed spasmogenic effects, and, therefore we do not think that these compounds could be involved in the spasmogenic activity.

α1-Adrenergic partial agonists utilize cytosolic Ca2+ more effectively for contraction in aortic smooth muscle

1990 ◽  
Vol 68 (10) ◽  
pp. 1329-1333 ◽  
Author(s):  
Issei Takayanagi ◽  
Shuji Onozuka
Keyword(s):  
Smooth Muscle ◽  
Key Words ◽  
Thoracic Aorta ◽  
Partial Agonist ◽  
Muscle Tension ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Tension Development ◽  
Aortic Smooth Muscle ◽  
Partial Agonists

Fura 2 loaded thoracic aorta strips from rabbits were used. Norepinephrine, phenylephrine, clonidine, and tizanidine induced an increase in cytosolic Ca2+ concentration ([Ca2+]i) and muscle tension in a concentration-dependent manner. A positive correlation between [Ca2+]i and tension development owing to the agonists was noted. The slope of regression lines between [Ca2+]i and tension development for clonidine and tizanidine, α1-adrenergic partial agonists, were significantly steeper than those for norepinephrine and phenylephrine, α1-adrenergic full agonists. The intrinsic activities of the partial agonists obtained from tension development were greater than those from changes in [Ca2+]i. These results suggest that the partial agonists cause a greater muscle tension than the full agonists at the same level of [Ca2+]i.Key words: cytosolic Ca2+ concentration, tension, partial agonist, full agonist,α1-adrenoceptors.

Neural and myogenic effects of leukotrienes C4, D4, and E4 on canine bronchial smooth muscle

1994 ◽  
Vol 266 (4) ◽  
pp. L414-L425 ◽  
Author(s):  
A. Abela ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Receptor Antagonist ◽  
Contractile Activity ◽  
Neuromuscular Control ◽  
Dependent Manner ◽  
Gamma Glutamyl Transpeptidase ◽  
Response Curves ◽  
Bronchial Smooth Muscle ◽  
Concentration Dependent Manner

The leukotrienes (LTs), referred to as the slow-reacting substance of anaphylaxis (SRS-A), are reported to have little or no activity in the canine airway. The objective of this study was to determine whether LTC4, LTD4, and LTE4 (10(-10)-10(-7) M) play a role in neuromuscular control of third- to fifth-order canine bronchi. In the presence of 1 microM indomethacin (Indo), canine bronchial smooth muscle contracted and was depolarized in a concentration-dependent manner by LTC4 or LTD4 but not by LTE4. LTC4 and LTD4 concentration-response curves were not significantly affected when conducted in the presence of any of the following: 10(-7) M propranolol (beta-adrenoceptor antagonist), 10(-6) M chlorpheniramine (H1-receptor antagonist), 10(-6) M ketanserin (nonselective 5-hydroxytryptamine receptor antagonist), 10(-7) M atropine (muscarinic receptor antagonist), and 10(-6) M tetrodotoxin (sodium channel blocker). LTC4 and LTD4 also potentiated electrical field-stimulated (EFS) excitatory junction potentials (EJPs), suggesting a possible prejunctional enhancement of acetylcholine release. In the absence of Indo, no postjunctional responses to LTC4 and LTD4 occurred. Endogenous prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha (a stable metabolite of PGI2) levels from canine bronchi were significantly reduced by Indo. In the presence of Indo, addition of > or = 10(-8) M of PGE2 suppressed contractions to LTC4 and LTD4. These data suggest that the decrease in PGE2 and PGI2 production by Indo is sufficient to unmask the excitatory postjunctional actions of LTC4 and LTD4 on bronchial smooth muscle. Serine borate (45 mM; an inhibitor of gamma-glutamyl transpeptidase, which prevents the conversion of LTC4 to LTD4) increased selectively the contractile activity of LTC4. L-Cysteine (3 mM; an inhibitor of an aminopeptidase, which prevents the conversion of LTD4 to LTE4) enhanced the contractile responses to LTD4. Serine borate increased the amplitude and duration of EFS contractions and potentiated the amplitude of EFS EJPs; the last effects were prevented by nordihydroguaiaretic acid. These and other studies suggest that LTs are synthesized by canine bronchi and have receptors on canine bronchial smooth muscle but that contractions to LTC4 and LTD4 in the canine airway are usually not observed because of the presence of inhibitory prostanoids (PGE2 and PGI2). We suggest that decreases in PGE2 and PGI2 in models of airway disease in combination with increases in LTC4, LTD4, and thromboxane A2 may contribute to airway hyperresponsiveness in vitro.

Effect of Volatile Anesthetics with and without Verapamil on Intracellular Activity in Vascular Smooth Muscle

1996 ◽  
Vol 84 (6) ◽  
pp. 1465-1474 ◽  
Author(s):  
Hitoshi Namba ◽  
Hideaki Tsuchida
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Muscle Tension ◽  
Volatile Anesthetics ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Pharmacomechanical Coupling ◽  
Intracellular Action

Background Although halothane and isoflurane inhibit receptor agonist-induced smooth muscle contraction by inhibiting Ca2+ influx via the L-type voltage-dependent Ca2+ channels, their effects on pharmacomechanical coupling remained to be clarified. The intracellular action of both anesthetics was studied during agonist-induced contractions using the Ca2+ channel blocker verapamil. Methods Isolated spiral strips of rat thoracic aorta with endothelium removed were suspended for isometric tension recordings in physiologic salt solution. Cytosolic concentration of Ca2+ ([Ca2+]i) was measured concomitantly using fura-2-Ca2+ fluorescence. Muscle contraction was evoked by the receptor agonists with 30 nm norepinephrine or 10 microM prostaglandin F2 alpha (PGF2 alpha), followed by exposure to halothane, at 0%, 1%, 2%, and 3% or isoflurane, at 2% and 4%. The effects of the anesthetics were compared with those of 0.1-1 microM verapamil (n = 8 for each condition). To clarify the intracellular action of the volatile anesthetics on agonist-induced contractions, this procedure was repeated for the anesthetics only in the presence of 1 microM verapamil (n = 8 for each condition). The effects of both anesthetics were also examined in nonreceptor-mediated contractions evoked with a 1-microM dose of the protein kinase C activator, 12-deoxyphorbol 13-isobutylate, which increases the Ca2+ sensitivity of the contractile elements (n = 8 for each). Results Halothane, isoflurane, and verapamil suppressed norepinephrine-and PGF2 alpha-induced increases in muscle tension and [Ca2+]i in a concentration-dependent manner. The Ca2+-tension regression lines suggested that the volatile anesthetics reduced Ca2+ sensitivity of the contractile elements during PGF2 alpha-induced contraction. Pretreatment of the muscle strip with verapamil revealed that halothane and isoflurane released Ca2+ during norepinephrine-induced contraction and that [Ca2+]i-tension relationship was modulated during PGF2 alpha-induced contractions. Halothane at 2% and 3% and isoflurane at 4% suppressed 12-deoxyphorbol 13-isobutylate-induced increases in muscle tension, whereas they enhanced increases in [Ca2+]i, indicating that both anesthetics suppressed Ca2+ sensitivity during 12-deoxyphorbol 13-isobutylate-induced contraction. Conclusions Verapamil pretreatment unmasked the intracellular action of the anesthetics. Halothane and isoflurane influenced pharmacomechanical coupling during agonist-induced contraction.

The indazole derivative YD-3 inhibits thrombin-induced vascular smooth muscle cell proliferation and attenuates intimal thickening after balloon injury

2004 ◽  
Vol 92 (12) ◽  
pp. 1232-1239 ◽  
Author(s):  
Jih-Hwa Guh ◽  
Yi-Nan Liu ◽  
Ya-Ling Chang ◽  
Sheng-Chu Kuo ◽  
Fang-Yu Lee ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Developmental Potential ◽  
Vsmc Proliferation ◽  
Neointimal Thickness ◽  
Immunochemical Detection

SummaryProliferation of vascular smooth muscle cells (VSMCs) is postulated to be one of the key events in the pathogenesis of atherosclerosis and restenosis. We investigated whether YD-3, a lowmolecular weight, non-peptide compound, could modulate proliferation of VSMCs in vitro and restenosis after balloon angioplasty in vivo. We examined the effect of YD-3 on thrombininduced VSMC proliferation by [3H]thymidine incorporation assay. The data demonstrated that YD-3 inhibited VSMC proliferation in a concentration-dependent manner. To define the mechanisms of YD-3 action, we found that YD-3 showed a profound inhibition on thrombin-induced Ras and ERK1/2 activities by using Western blotting analysis. Furthermore, oral administration of YD-3 exhibited a marked reduction in neointimal thickness using the carotid injury model in rats. Using immunochemical detection, our experiments also revealed that YD-3 significantly suppressed expression of the PAR-1 receptor, and markedly inhibited PAR-1-activating peptide (SFLLRN)-induced VSMC proliferation in a concentration-dependent manner. These results suggest that YD-3 inhibits thrombin-induced VSMC growth via the Rasand ERK1/2-mediated signaling pathway. Moreover, YD-3 also shows a developmental potential in the treatment of atherosclerosis and restenosis after vascular injury.

Serotonin 5-HT7 receptors mediate relaxation of porcine pial veins

2000 ◽  
Vol 278 (3) ◽  
pp. H907-H912 ◽  
Author(s):  
Takaaki Ishine ◽  
Isabelle Bouchelet ◽  
Edith Hamel ◽  
Tony J. F. Lee
Keyword(s):  
Smooth Muscle ◽  
Muscle Tone ◽  
Receptor Gene ◽  
Receptor Subtype ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Rhythmic Contractions ◽  
High Degree ◽  
Pcr Techniques

Isolated porcine pial veins in the presence of active muscle tone have been shown to exhibit rhythmic contractions (RC) that are inhibited by serotonin (5-HT) in a concentration-dependent manner. The 5-HT inhibition of RC is mediated by an as yet unidentified 5-HT receptor subtype located on the vascular smooth muscle. 5-carboxamidotryptamine, which is a potent but nonselective agonist at 5-HT7receptors, has been shown to be the most potent inhibitor of RC in porcine pial veins. Therefore, the present study was designed to determine if the 5-HT-mediated inhibition of RC in pial veins is mediated by 5-HT7 receptors and if 5-HT7 receptor mRNA is expressed in endothelium-denuded pial veins; the study was done with the use of an in vitro tissue bath and RT-PCR techniques. Our findings indicated that 5-HT inhibition of RC in porcine pial veins was prevented by 5-HT7-receptor antagonists (clozapine, pimozide, and LY-215840) in a concentration-dependent manner. Furthermore, a strong PCR signal for the 5-HT7 receptor was consistently detected in endothelium-denuded pial veins. Sequence analysis of the amplified products confirmed their high degree of homology with the porcine and/or human 5-HT7-receptor gene. Taken together, these data suggest that the 5-HT-induced inhibition of RC in porcine pial veins is at least in part mediated by 5-HT7 receptors located on the venous smooth muscle.

Sign in / Sign up

Export Citation Format

Share Document