Arecoline excites the contraction of distal colonic smooth muscle strips in rats via the M3 receptor – extracellular Ca2+ influx – Ca2+ store release pathway

2010 ◽  
Vol 88 (4) ◽  
pp. 439-447 ◽  
Author(s):  
Chuan-Bao Li ◽  
Xiao Yang ◽  
Wen-Bo Tang ◽  
Chuan-Yong Liu ◽  
Dong-Ping Xie
Keyword(s):  
Smooth Muscle ◽  
Longitudinal Muscle ◽  
Contractile Response ◽  
Circular Muscle ◽  
Distal Colon ◽  
Dependent Manner ◽  
Krebs Solution ◽  
Chinese Herbal ◽  
M3 Receptor ◽  
Dose Dependent

Areca is a Chinese herbal medicine that is widely used for constipation. However the mechanisms of its action are not clear. We investigated the effects of arecoline, the most active component of areca, on the motility of rat distal colonic smooth muscle strips. In longitudinal muscle of distal colon (LMDC) and circular muscle of distal colon (CMDC), arecoline increased the contraction in a dose-dependent manner. Tetrodotoxin (TTX) did not inhibit the effects of arecoline. The contractile response to arecoline was completely antagonized by atropine. 4-Diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) strongly depressed the response to arecoline, but gallamine and methoctramine did not. Nifedipine, 2-aminoethoxydiphenyl borate (2-APB), and Ca2+-free Krebs solution with EGTA partly inhibited the effects of arecoline. The sum of Ca2+-free Krebs solution, EGTA, and 2-APB completely inhibited the effects of arecoline. The results show that arecoline stimulates distal colonic contraction in rats via the muscarinic (M3) receptor – extracellular Ca2+ influx – Ca2+ store release pathway. It is likely that the action of areca in relieving constipation is due to its stimulation of muscle contraction.

The role of transmembrane sodium gradient in rabbit ileal smooth muscle: Utilization of harmaline

1985 ◽  
Vol 5 (8) ◽  
pp. 667-671 ◽  
Author(s):  
M. S. Suleiman
Keyword(s):  
Smooth Muscle ◽  
Contractile Response ◽  
Sodium Concentration ◽  
Exchange Mechanism ◽  
Dependent Manner ◽  
Sodium Gradient ◽  
Extracellular Sodium ◽  
Dose Dependent

Decreasing extracellular sodium concentration was found to produce a contractile response of rabbit ileal smooth muscle. As the concentration decreases, the amplitude of contraction increases, thus producing a dose-dependent curve. Harmaline, a competitor for sodium, was found to inhibit the sodium gradient-dependent contractions in a dose-dependent manner. The results are interpreted as harmaline inhibiting a Na–Ca exchange mechanism present in ileal smooth muscle.

Effects of cholecystokinin-octapeptide on gastric motility of anesthetized dogs

1986 ◽  
Vol 251 (5) ◽  
pp. G678-G681 ◽  
Author(s):  
A. Kuwahara ◽  
K. Ozawa ◽  
N. Yanaihara
Keyword(s):  
Smooth Muscle ◽  
Gastric Motility ◽  
Contractile Response ◽  
Smooth Muscle Contraction ◽  
Dependent Manner ◽  
Local Effects ◽  
Cholecystokinin Octapeptide ◽  
Gastric Smooth Muscle ◽  
Anesthetized Dogs ◽  
Dose Dependent

The present experiments examined the local effects of cholecystokinin-octapeptide (CCK-8) and related peptides on gastric motility of anesthetized dogs. Peptides were injected through the gastroepiploic artery at doses of 1.0, 2.5, 5.0, 10.0, and 20.0 ng/ml. CCK-8 and its analogues (Glt-CCK-8, pGlu-CCK-8, and Suc1-MePhe8-CCK-7) increased gastric smooth muscle contraction in a dose-dependent manner. ED50 of CCK-8 was 2.97 +/- 0.63 ng/ml. Administration of atropine (100–200 micrograms/kg) inhibited the effects of both CCK-8 and pentagastrin; however, hexamethonium (5 mg/kg) failed to block the contractile response induced by CCK-8 and pentagastrin. These results indicate that CCK-8 and related peptides can act as local modulators in controlling the neural regulation of gastric motility.

Distribution of beta-adrenoceptors associated with cAMP-generating system in cat colon

1987 ◽  
Vol 253 (3) ◽  
pp. G378-G382 ◽  
Author(s):  
K. Taniyama ◽  
T. Kuno ◽  
C. Tanaka
Keyword(s):  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Beta Adrenoceptors ◽  
Auerbach’S Plexus ◽  
Camp Levels ◽  
Dose Dependent ◽  
Auerbach's Plexus ◽  
Generating System

The localization of beta-adrenoceptor associated with the adenosine 3',5'-cyclic monophosphate (cAMP)-generating system was determined by an assessment of the smooth muscle cell contractility and by assay of cAMP in individual layers of the cat colon. Isoproterenol inhibited the acetylcholine (ACh)-induced contractions of isolated longitudinal and circular muscle cells in a dose-dependent manner. The response of the longitudinal muscle cells to isoproterenol was double that seen in the circular muscle cells, and this inhibition was antagonized by sotalol. The basal content of cAMP was 3.42 pmol/mg protein in longitudinal muscle layers, 3.09 pmol/mg protein in circular muscle layers, and 2.75 pmol/mg protein in Auerbach's plexus. Isoproterenol produced a dose-dependent elevation of cAMP levels in longitudinal and circular muscle layers, which were antagonized by sotalol and potentiated by theophylline. By contrast, isoproterenol had no effect on cAMP in Auerbach's plexus. Phenylephrine did not alter the cAMP levels in any layer. Therefore, beta-adrenoceptors associated with the cAMP-generating system probably exist in the longitudinal and circular muscles of the cat colon.

Role of extracellular calcium and calmodulin in prolactin secretion induced by hyposmolarity, thyrotropin-releasing hormone, and high K+ in GH4C1 cells

1990 ◽  
Vol 123 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Xiangbing Wang ◽  
Noriyuki Sato ◽  
Monte A. Greer ◽  
Susan E. Greer ◽  
Staci McAdams
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxant ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Dependent Manner ◽  
Cell Toxicity ◽  
High K ◽  
Dose Dependent ◽  
Smooth Muscle Relaxant

Abstract. The mechanism by which 30% medium hyposmolarity induces PRL secretion by GH4C1 cells was compared with that induced by 100 nmol/l TRH or 30 mmol/l K+. Removing medium Ca2+, blocking Ca2+ channels with 50 μmol/l verapamil, or inhibiting calmodulin activation with 20 μmol/l trifluoperazine, 10 μmol/l chlorpromazine or 10 μmol/l pimozide almost completely blocked hyposmolarity-induced secretion. The smooth muscle relaxant, W-7, which is believed relatively specific in inhibiting the Ca2+-calmodulin interaction, depressed hyposmolarity-induced PRL secretion in a dose-dependent manner (r = −0.991, p<0.01 ). The above drugs also blocked or decreased high K+-induced secretion, but had much less effect on TRH-induced secretion. Secretion induced by TRH, hyposmolarity, or high K+ was optimal at pH 7.3-7.65 and was significantly depressed at pH 6.0 or 8.0, indicating that release of hormone induced by all 3 stimuli is due to an active cell process requiring a physiologic extracellular pH and is not produced by nonspecific cell toxicity. The data suggest hyposmolarity and high K+ may share some similarities in their mechanism of stimulating secretion, which is different from that of TRH.

The Morphology of the Gut of the Brown Trout (Salmo trutta)

1959 ◽  
Vol s3-100 (50) ◽  
pp. 183-198
Author(s):  
G. BURNSTOCK
Keyword(s):  
Smooth Muscle ◽  
Salmo Trutta ◽  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Living System ◽  
Cardiac Stomach ◽  
Longitudinal Smooth Muscle ◽  
Brown Trout Salmo Trutta ◽  
Pyloric Stomach ◽  
Longitudinal Layer

1. In the trout gut a short oesophagus containing only striated circular muscles opens into a large cardiac stomach possessing inner circular and outer longitudinal smooth muscle-coats, as well as a musculsris mucosse. Ahout 45 pyloric caeca come off the intestine, which, while containing muscle-coats, does not possess a muscularis mucosae. In the rectum, the longitudinal muscle is as thick as the circular muscle-coat, hut in other regions the circular muscle is dominant, especially in the pyloric stomach where it is over 10 times as thick ss the longitudinal layer. 2. The mucosa is distinguished by the presence of a prominent layer of dense collagen, the stratum compactum, which is perforated only by nerves and blood-vessels. This layer forms a firm and relatively inextensible (approximately 10% extensibility) basis to the gut-wall. It limits the extensibility of the smooth muscle to 75% radially in the stomach and 25% radially and longitudinally in the intestine. In contrast, the stomachs of the pike and perch, which do not possess a stratum compactum, extend up so 200%. 3. A detailed description of the regional junctions and sphincters gives a basis for the interpretation of events occurring in the living system. Valves at the junction of the pneumatic duct with the oesophagus, and between the duodenum and pyloric stomach, serve to prevent the regurgitation of gas and semi-digested food respectively. A complex sphincter mechanism exists at the pylorus, and to a lesser extent at the antrum. A series of about five circular muscle-constrictors represents the anus. 4. It is suggested that the cells forming the stratum granulosum, a layer closely associated with the stratum compactum, are composed of active fibroblast cells producing collagen. 5. The rectum contains a muscular annulo-spiral septum of unknown function which protrudes into the lumen.

Membrane currents recorded from a fragment of rabbit intestinal smooth muscle cell

1986 ◽  
Vol 251 (3) ◽  
pp. C335-C346 ◽  
Author(s):  
Y. Ohya ◽  
K. Terada ◽  
K. Kitamura ◽  
H. Kuriyama
Keyword(s):  
Smooth Muscle ◽  
Longitudinal Muscle ◽  
Outward Current ◽  
Ionic Currents ◽  
Muscle Layer ◽  
Dependent Manner ◽  
Rabbit Ileum ◽  
Longitudinal Muscle Layer ◽  
Inward Current ◽  
K Currents

Properties of ionic currents in smooth muscle membranes of the longitudinal muscle layer of the rabbit ileum were investigated using the single electrode voltage clamp method. In the present experiments, this method was applicable only to the smooth muscle ball (fragment) and not for the dispersed whole cell, because of incompleteness of the voltage clamping. A voltage step elicited a transient inward current followed by an outward current. This outward current was partly inhibited by Mn2+ or nisoldipine or by a reduction in the extracellular [Ca2+] ([Ca2+]o). Tetraethylammonium (TEA) reduced the delayed outward current in a dose-dependent manner, but 50 mM TEA did not produce a complete block of a residual current. When the pipette contained K+-free (Cs+ with TEA+) solution, the residual outward current was abolished. The inward current was elicited at -30 mV (holding potential of -60 mV) and reached the maximal value at +10 mV; the polarity was reversed at +60 mV. This inward current depended on the [Ca2+]o and was blocked by Mn2+ or nisoldipine. Ba2+ also permeated the membrane, and the inward current evoked by Ba2+ was also blocked by Mn2+ or nisoldipine. Reduction of [Na+]o in a solution containing 2.4 mM Ca2+ neither modified the current-voltage relation nor the decay of the inward current, but when [Ca2+]o was reduced to below 1 microM, Na+ permeated the membrane and was blocked by nisoldipine. In conclusion, ionic currents were recordable from the fragmented ball of the longitudinal muscle of rabbit ileum. There were at least two K+ currents as the outward current (Ca2+-dependent K+ and delayed K+ currents) and a Ca2+ current as the inward current. The property of the Ca2+ channel was similar to that observed with other preparations.

Rho activation in excitatory agonist-stimulated vascular smooth muscle

2001 ◽  
Vol 281 (2) ◽  
pp. C571-C578 ◽  
Author(s):  
Sotaro Sakurada ◽  
Hiroyuki Okamoto ◽  
Noriko Takuwa ◽  
Naotoshi Sugimoto ◽  
Yoh Takuwa
Keyword(s):  
Smooth Muscle ◽  
Kinase Inhibitor ◽  
Contractile Response ◽  
Rho Kinase ◽  
Small Gtpase ◽  
Dependent Manner ◽  
Aortic Smooth Muscle ◽  
Rhoa Activation ◽  
Downstream Effector ◽  
First Time

Small GTPase Rho and its downstream effector, Rho kinase, have been implicated in agonist-stimulated Ca2+ sensitization of 20-kDa myosin light chain (MLC20) phosphorylation and contraction in smooth muscle. In the present study we demonstrated for the first time that excitatory receptor agonists induce increases in amounts of an active GTP-bound form of RhoA, GTP-RhoA, in rabbit aortic smooth muscle. Using a pull-down assay with a recombinant RhoA-binding protein, Rhotekin, we found that a thromboxane A2 mimetic, U-46619, which induced a sustained contractile response, induced a sustained rise in the amount of GTP-RhoA in a dose-dependent manner with an EC50 value similar to that for the contractile response. U-46619-induced RhoA activation was thromboxane A2 receptor-mediated and reversible. Other agonists including norepinephrine, serotonin, histamine, and endothelin-1 (ET-1) also stimulated RhoA, albeit to lesser extents than U-46619. In contrast, ANG II and phorbol 12,13-dibutyrate failed to increase GTP-RhoA. The tyrosine kinase inhibitor genistein substantially inhibited RhoA activation by these agonists, except for ET-1. Thus excitatory agonists induce Rho activation in an agonist-specific manner, which is thought to contribute to stimulation of MLC20 phosphorylation Ca2+ sensitivity.

Intracellular pathways for contraction in gastroesophageal smooth muscle cells

1991 ◽  
Vol 260 (5) ◽  
pp. G770-G775 ◽  
Author(s):  
C. Hillemeier ◽  
K. N. Bitar ◽  
J. M. Marshall ◽  
P. Biancani
Keyword(s):  
Smooth Muscle ◽  
Salt Solution ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Free Medium ◽  
Calmodulin Antagonists ◽  
Intact Cells ◽  
Intact Muscle ◽  
Intracellular Pathways ◽  
Dose Dependent

Intracellular pathways utilized for contraction in response to acetylcholine (ACh), inositol 1,4,5-trisphosphate (IP3), and KCl were examined in isolated circular smooth cells from the esophagus, lower esophageal sphincter (LES), and fundus. In physiological nutrient salt solution (PSS) intact muscle cells isolated from these three tissues responded in a similar dose-dependent manner to ACh. In all tissues the contractile response to ACh was maximal at 30 s. Contraction of smooth muscle cells from LES and fundus did not change after incubation in Ca(2+)-free medium, but contraction of esophageal cells was abolished. KCl-induced contraction of all three cell types was also abolished after incubation in Ca(2+)-free medium. After permeabilization with saponin in cytosolic (low Ca2+) salt solution, muscle cells from LES and fundus contracted in a dose-dependent manner in response to IP3, whereas cells from esophagus did not contract. Contraction of permeabilized LES and fundic cells in response to ACh was the same as that of intact muscle cells. Response to IP3 was more rapid than response to ACh; it reached 85% of maximum by 5 s and peaked at 15 s. Calmodulin antagonists W-7 and CGS 9343B blocked contraction in response to ACh in intact cells from LES and fundus but had no effect on ACh-induced contraction in esophageal cells. These antagonists blocked IP3-induced contraction in permeabilized cells from LES and fundus. KCl-induced contraction in intact cells from all three tissues was not blocked by either W-7 or CGS 9343B. These data suggest that calmodulin antagonists block contraction mediated by release of intracellular Ca2+ induced by ACh or IP3.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of the effects of neurokinins on canine antral muscle

1988 ◽  
Vol 255 (6) ◽  
pp. G779-G786
Author(s):  
C. B. Koelbel ◽  
E. A. Mayer ◽  
G. van Deventer ◽  
W. J. Snape ◽  
A. Patel
Keyword(s):  
Substance P ◽  
Mechanical Response ◽  
Longitudinal Muscle ◽  
Rank Order ◽  
Circular Muscle ◽  
Neurokinin A ◽  
Inotropic Response ◽  
Chronotropic Response ◽  
Natural Ligand ◽  
Dose Dependent

The excitation of longitudinal antral muscle by substance P (SP) involves both a myogenic and a cholinergic effect. To examine if these responses are mediated by different neurokinin receptors, we studied the mechanical response and the release of [3H]acetylcholine from antral muscle strips in response to SP, substance P methylester (SPME), neurokinin A (NKA), neurokinin B (NKB), and several non-mammalian tachykinins. All peptides studied showed a dose-dependent inotropic and chronotropic effect on spontaneous phasic contractions. This ionotropic effect in longitudinal muscle was partially atropine sensitive for SPME, SP, and NKB but not for NKA, whereas neither atropine nor tetrodotoxin had an effect in circular muscle. In longitudinal muscle, all three neurokinins were equipotent. In longitudinal muscle treated with atropine and in circular muscle, the rank order of potency for the inotropic response was NKA greater than NKB greater than SP greater than SPME. For the chronotropic response the rank order was SPME, SP greater than NKA greater than NKB. NKA, NKB, and SP caused a dose-dependent, tetrodotoxin-sensitive increase in [3H]acetylcholine release from strips preincubated with [3H]choline. NKA was significantly more potent to release [3H]acetylcholine than either NKB or SP. The stimulated release was inhibited by [D-Ala2,D-Met5]methionine enkephalinamide and the SP antagonist, spantide. These results are consistent with the hypothesis that NKA is the natural ligand mediating the myogenic inotropic response in both muscle layers and the cholinergic response in longitudinal muscle.

Voltage sensitivity of slow wave frequency in isolated circular muscle strips from guinea pig gastric antrum

1999 ◽  
Vol 276 (2) ◽  
pp. G518-G528 ◽  
Author(s):  
S.-M. Huang ◽  
S. Nakayama ◽  
S. Iino ◽  
T. Tomita
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Slow Wave ◽  
Circular Muscle ◽  
Gastric Antrum ◽  
Slow Waves ◽  
Wave Frequency ◽  
Voltage Sensitivity ◽  
Dependent Manner ◽  
Circular Smooth Muscle

In circular muscle preparations isolated from the guinea pig gastric antrum, regular spontaneous electrical activity (slow waves) was recorded. Under normal conditions (6 mM K+), the frequency and shape of the slow waves were similar to those observed in ordinary stomach smooth muscle preparations. When the resting membrane potential was hyperpolarized and depolarized by changing the extracellular K+ concentration (2–18 mM), the frequency of slow waves decreased and increased, respectively. Application of cromakalim hyperpolarized the cell membrane and reduced the frequency of slow waves in a dose-dependent manner. Cromakalim (3 μM) hyperpolarized the membrane, and slow waves ceased in most preparations. In the presence of cromakalim, subsequent increases in the extracellular K+ concentration restored the frequency of slow waves accompanied by depolarization. Also, glibenclamide completely antagonized this effect of cromakalim. In smooth muscle strips containing both circular and longitudinal muscle layers, such changes in the slow wave frequency were not observed. It was concluded that the maneuver of isolating circular smooth muscle altered the voltage dependence of the slow wave frequency.

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