scholarly journals Characteristics of the muscularis mucosae in the acid-secreting region of the rabbit stomach

1999 ◽  
Vol 276 (5) ◽  
pp. G1213-G1220 ◽  
Author(s):  
W. H. Percy ◽  
J. M. Warren ◽  
J. T. Brunz
Keyword(s):  
Acid Secretion ◽  
Electrical Field Stimulation ◽  
Muscularis Mucosae ◽  
Regional Variability ◽  
Electrical Field ◽  
Intrinsic Nerve ◽  
Gastric Corpus ◽  
Acid Secreting ◽  
Acid Release

It has been suggested that muscularis mucosae excitation may augment gastric acid secretion, implying that this muscle should contract to secretagogues or stimulation of its motor innervation. The aim of this study was to characterize in vitro the responses of the muscularis mucosae in the rabbit gastric corpus to substances that modulate acid release and to intrinsic nerve stimulation. Muscularis mucosae from both fundic and antral ends of the corpus had identical mechanical properties, contracted to ACh, ADP, ATP, and histamine but relaxed to vasoactive intestinal polypeptide. Fundic but not antral muscularis mucosae contracted to bombesin and PGE2and PGF2α, whereas adenosine, AMP, CCK, gastrin, secretin, and somatostatin were without effect on any preparation. In both regions electrical field stimulation evoked TTX-sensitive responses consisting of an atropine-resistant contraction followed by an N G-nitro-l-arginine methyl ester- and indomethacin-resistant relaxation. It is concluded from the regional variability in the pharmacological properties of the gastric muscularis mucosae that if its motor activity is linked to acid secretion this would be achieved by a neurally mediated relaxation rather than a paracrine- and/or endocrine-induced alteration in tone.

Multiple responses to electrical field stimulation in circular muscle of canine gastric corpus

1984 ◽  
Vol 62 (8) ◽  
pp. 912-918 ◽  
Author(s):  
Yasushi Sakai ◽  
Edwin E. Daniel
Keyword(s):  
Substance P ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Scorpion Venom ◽  
Adrenergic Blockade ◽  
Field Stimulation ◽  
Electrical Field ◽  
Gastric Corpus

Innervation of circular muscle of the canine stomach studied in vitro was investigated by subjecting muscle strips to electrical field stimulation. Strips were cut from the lesser curvature of the gastric corpus and stimulated with 10-s trains of 0.5-ms pulses at 0.5–20 Hz, 40 V. Most responses were classified into one of three types. In general, field stimulation tended to elicit sequences of varying magnitudes of transient on-contraction, on-relaxation, off-relaxation, off-contraction. Responses were abolished by tetrodotoxin. On-contraction was almost abolished by atropine plus desensitization by 5-hydroxytryptamine (5-HT) or substance P. On-relaxation and off-relaxation were not affected by adrenergic blockade, methysergide, apamin, or 4-aminopyridine. ATP usually caused contraction and slightly diminished relaxation to field stimulation. Vasoactive intestinal polypeptide (VIP) had little effect on tone and response to field stimulation. Relaxation disappeared after scorpion venom treatment. This probably resulted from depletion of the transmitter which mediates relaxation. Off-contraction was reduced by atropine, desensitization by 5-HT or substance P, cromoglycate, indomethacin or ATP, but was not affected by adrenergic blockade, hexamethonium, methysergide, mepyramine, or VIP. The findings suggest that innervation of gastric corpus circular muscle included excitatory cholinergic and both excitatory and inhibitory noncholinergic, nonadrenergic innervation. However, the responses of circular muscle to field stimulation in vitro were drastically different from those obtained previously in vivo, suggesting damage or altered inputs to circular muscle when strips of circular muscle are studied.

Pharmacological characterization of opossum distal colonic muscularis mucosae in vitro

1986 ◽  
Vol 250 (1) ◽  
pp. G98-G102 ◽  
Author(s):  
W. H. Percy ◽  
J. Christensen
Keyword(s):  
Electrical Field Stimulation ◽  
Distal Colon ◽  
Field Stimulation ◽  
Muscularis Mucosae ◽  
Electrical Field ◽  
Pharmacological Characterization ◽  
Neural Inhibition ◽  
Spontaneous Contractions

In muscularis mucosae from the opossum distal colon, both tone and spontaneous contractions were highly dependent on the available oxygen. Acetylcholine and histamine caused, respectively, atropine- and pyrilamine-sensitive contractions. Norepinephrine relaxed the tissue, an effect abolished by propranolol. Under these conditions norepinephrine failed to elicit contractions and at higher concentrations again caused relaxations. The tissue gave concentration-dependent relaxations to ATP but not to ADP, AMP, or adenosine. Electrical field stimulation (20-30 Hz, 1-2 ms, 120 mA) revealed a cholinergic excitatory innervation and a nonadrenergic, noncholinergic neural inhibition. Cholecystokinin, gastrin, substance P, and vasoactive intestinal polypeptide were without effect on this tissue. In these respects, colonic muscularis mucosae differs considerably from that of other gastrointestinal viscera.

Release of epithelium-derived PGE2 from canine trachea after antigen inhalation

1998 ◽  
Vol 274 (2) ◽  
pp. L220-L225 ◽  
Author(s):  
I. McGrogan ◽  
L. J. Janssen ◽  
J. Wattie ◽  
P. M. O’Byrne ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Electrical Field Stimulation ◽  
Tracheal Smooth Muscle ◽  
Organ Bath ◽  
Field Stimulation ◽  
Electrical Field ◽  
Concentration Response Curve

To investigate the role of prostaglandin (PG) E2 in allergen-induced hyperresponsiveness, dogs inhaled either the allergen Ascaris suum or vehicle (Sham). Twenty-four hours after inhalation, some animals exposed to allergen demonstrated an increased responsiveness to acetylcholine challenge in vivo (Hyp-Resp), whereas others did not (Non-Resp). Strips of tracheal smooth muscle, either epithelium intact or epithelium denuded, were suspended on stimulating electrodes, and a concentration-response curve to carbachol (10−9 to 10−5 M) was generated. Tissues received electrical field stimulation, and organ bath fluid was collected to determine PGE2content. With the epithelium present, all three groups contracted similarly to 10−5 M carbachol, whereas epithelium-denuded tissues from animals that inhaled allergen contracted more than tissues from Sham dogs. In response to electrical field stimulation, Hyp-Resp tissues contracted less than Sham tissues in the presence of epithelium and more than Sham tissues in the absence of epithelium. PGE2release in the muscle bath was greater in Non-Resp tissues than in Sham or Hyp-Resp tissues when the epithelium was present. Removal of the epithelium greatly inhibited PGE2release. We conclude that tracheal smooth muscle is hyperresponsive in vitro after in vivo allergen exposure only when the modulatory effect of the epithelium, largely through PGE2 release, is removed.

Nonadrenergic inhibitory nervous system in human airways

1976 ◽  
Vol 41 (5) ◽  
pp. 764-771 ◽  
Author(s):  
J. Richardson ◽  
J. Beland
Keyword(s):  
Smooth Muscle ◽  
Gastrointestinal Tract ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Inhibitory System ◽  
Electrical Field ◽  
Human Airways ◽  
Adrenergic Blocking ◽  
Stimulation Of

Human airways, from the middle of the trachea to the distal bronchi, were studied in vitro for the presence of inhibitory nerves. The tissue was obtained from operations and from recent autopsies. Electrical field stimulation of the tissues demonstrated cholinergic, excitatory nerves and their effect was blocked by atropine. Field stimulation of the tissues, in the presence of atropine, relaxed the smooth muscle even when the muscle was contracted by histamine. The field stimulation-induced relaxation was neither blocked nor modified by adrenergic blocking agents. Maximum relaxation of the bronchial muscle was obtained with a pulse duration of 1–2 ms, 70 V,and frequencies of 20 Hz and greater. The tracheal smooth muscle showed 85%of maximal relaxation with a frequency of 10 Hz. Tetrodotoxin, blocked the field stimulation-induced relaxation for pulse durations of 2 ms; this indicated that nerves were being stimulated. The airway system shows some of the characteristics of the nonadrenergic inhibitory system in the gastrointestinal tract and of the system reported in the guinea pig trachealis muscle.No evidence of adrenergic inhibitory fibers was found in the bronchial muscle with either pharmacological or histochemical techniques. These findings suggest that the nonadrenergic inhibitory system is the principal inhibitory system for the smooth muscle of human airways. We suggest that a defect in the airway system, such as that shown in the gastrointestinal tract, may be an explanation for the hyperreactive airways of asthma and chronic bronchitis.

Maturation of nonadrenergic noncholinergic inhibitory system in normal and allergen-sensitized rabbits

1994 ◽  
Vol 267 (6) ◽  
pp. L739-L744 ◽  
Author(s):  
G. N. Colasurdo ◽  
J. E. Loader ◽  
J. P. Graves ◽  
G. L. Larsen
Keyword(s):  
Electrical Field Stimulation ◽  
Neurokinin A ◽  
Inhibitory System ◽  
Electrical Field ◽  
New Zealand White Rabbits ◽  
Parenteral Exposure ◽  
The Mean ◽  
Nanc Relaxation ◽  
Specific Allergen

We investigated the functional existence of the nonadrenergic noncholinergic inhibitory (NANCi) system in developing rabbit airways in vitro. Furthermore, we evaluated the effect of parenteral exposure to a specific allergen (ragweed) on the maturation of this neural pathway. NANCi responses were studied on tracheal smooth muscle (TSM) segments obtained from normal and ragweed-sensitized New Zealand White rabbits at 1, 2, 4, and 12 wk of age. The TSM segments were removed and placed in tissue baths containing modified Krebs-Henseleit solution, atropine (1 x 10(-5) M), and propranolol (5 x 10(-6) M). After contraction with neurokinin A (1 x 10(-5) M), electrical field stimulation was applied at stimulation frequencies ranging from 5 to 30 Hz to determine the frequency that produced maximal relaxation. The NANCi response to EFS was measured and expressed as the mean (+/- SE) percent relaxation at 20 Hz, because this stimulation frequency gave the maximal NANCi response at each age studied. TSM segments obtained from control rabbits at 1 wk of age did not demonstrate a NANCi response at the frequencies of stimulation used. By contrast, a reproducible NANC relaxation was demonstrated in TSM from 2-, 4-, and 12-wk-old rabbits. The magnitude of this response was 27 +/- 4.7 (n = 10), 29 +/- 4.8 (n = 9), and 37 +/- 4% (n = 18), respectively. The same experiments performed on TSM segments obtained from ragweed-sensitized animals gave significantly decreased values of NANCi response. In 2-, 4-, and 12-wk-old rabbits, the NANCi responses were 11.5 +/- 3.4 (n = 9), 11 +/- 2 (n = 13), and 16 +/- 4.2% (n = 14).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway smooth muscle responsiveness from dogs with airway hyperresponsiveness after O3 inhalation

1988 ◽  
Vol 65 (1) ◽  
pp. 57-64 ◽  
Author(s):  
G. L. Jones ◽  
P. M. O'Byrne ◽  
M. Pashley ◽  
R. Serio ◽  
J. Jury ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Potassium Chloride ◽  
Airway Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field ◽  
Trachealis Muscle

Airway hyperresponsiveness occurs after inhalation of O3 in dogs. The purpose of this study was to examine the responsiveness of trachealis smooth muscle in vitro to electrical field stimulation, exogenous acetylcholine, and potassium chloride from dogs with airway hyperresponsiveness after inhaled O3 in vivo and to compare this with the responsiveness of trachealis muscle from control dogs. In addition, excitatory junction potentials were measured with the use of single and double sucrose gap techniques in both groups of dogs to determine whether inhaled O3 affects the release of acetylcholine from parasympathetic nerves in trachealis muscle. Airway hyperresponsiveness developed in all dogs after inhaled O3 (3 ppm for 30 min). The acetylcholine provocative concentration decreased from 4.11 mg/ml before O3 inhalation to 0.66 mg/ml after O3 (P less than 0.0001). The acetylcholine provocative concentration increased slightly after control inhalation of dry room air. Airway smooth muscle showed increased responses to both electrical field stimulation and exogenous acetylcholine but not to potassium chloride in preparations from dogs with airway hyperresponsiveness in vivo. The increased response to electrical field stimulation was not associated with a change in excitatory junctional potentials. These results suggest that a postjunctional alteration in trachealis muscle function occurs after inhaled O3 in dogs, which may account for airway hyperresponsiveness after O3 in vivo.

Differential tachykinin receptor subtype activation in capsaicin and KCl contractions of guinea pig trachealis

1995 ◽  
Vol 269 (6) ◽  
pp. L837-L842
Author(s):  
R. W. Mitchell ◽  
I. M. Ndukwu ◽  
A. Herrnreiter ◽  
K. Uzendoski ◽  
B. Gitter ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Electrical Field Stimulation ◽  
Receptor Subtype ◽  
Nk1 Receptor ◽  
Electrical Field ◽  
Tachykinin Receptor ◽  
Nk1 Receptor Antagonist

We assessed the role of endogenously secreted tachykinins in mediating contraction caused by potassium chloride (KCl) in guinea pig tracheal smooth muscle (TSM) strips in vitro. Maximal isometric contraction was elicited with approximately 45 mM KCl and was 196 +/- 8% of the response to electrical field stimulation (% EFS) in the same tissues. Muscarinic receptor blockade with atropine modestly attenuated this contraction caused by KCl to 175 +/- 9 %EFS (P < 0.05), and treatment with a selective neurokinin subtype 1 (NK1) receptor antagonist, LY-297911, caused even greater inhibition of KCl-elicited contraction to 124 +/- 8 %EFS (P < 0.001). By contrast, SR-48968, a selective NK2 antagonist, had no effect on contraction caused by KCl (183 +/- 9 %EFS; P = NS vs. KCl alone). However, given together at the same concentration, SR-48968 augmented the inhibition of contraction caused by LY-297911 to 93 +/- 15 %EFS (P < 0.05 vs. LY-297911 alone). In contrast to the effect on KCl-induced contraction, LY-297911 caused only moderate inhibition of the contraction caused by capsaicin to 81 +/- 13 %EFS (P < 0.05 vs. control, 114 +/- 15 %EFS), whereas SR-48968 caused substantial attenuation of contraction caused by capsaicin to 23 +/- 5 %EFS (P < 0.005 vs. LY-297911). We demonstrate that a significant portion of the contraction caused by KCl, in addition to capsaicin, is elicited in guinea pig TSM through neurokinin secretion. However, NK1 receptors predominantly mediate contraction caused by KCl, and NK2 receptors predominantly mediate contraction elicited by capsaicin in guinea pig airway smooth muscle.

Mechanism underlying ozone-induced in vitro hyperresponsiveness in canine bronchi

1991 ◽  
Vol 261 (2) ◽  
pp. L55-L62
Author(s):  
L. J. Janssen ◽  
P. M. O'Byrne ◽  
E. E. Daniel
Keyword(s):  
Airway Hyperresponsiveness ◽  
Electrical Field Stimulation ◽  
Progressive Decrease ◽  
Electrical Field ◽  
Thromboxane Receptor ◽  
Direct Measurements ◽  
Thromboxane Receptor Antagonist ◽  
Over Time

The effects of ozone inhalation on the contractility of canine bronchi and the mechanisms underlying any changes observed were investigated. Ozone inhalation caused acetylcholine airway hyperresponsiveness in vivo. Isolated segments of bronchi (3rd to 5th order) from dogs previously exposed to ozone (or normal air) were mounted in organ baths. Contractile responses to electrical field stimulation (FS) in all tissues decreased in magnitude over time (measured at 10, 120, 210, and 300 min after mounting tissues in the organ baths); responses to 150 mM KCl did not show such a progressive decrease. Ozone inhalation produced a dramatic enhancement of FS responses, a smaller enhancement of responses to carbachol (10(-8)-10(-4) M), and no change in responses to KCl (150 mM). In the presence of 10(-5) M indomethacin, all responses were enhanced and tended to increase in magnitude over time; indomethacin also abolished the differences in responsiveness between the control and ozone-exposed tissues. In the presence of the thromboxane receptor antagonist L-670,596 (10(-8) M), the magnitudes of all FS responses showed a progressive decrease over time while KCl responses did not; again, the differences in FS responses between control and ozone-exposed tissues were decreased or made insignificant. In conclusion, ozone produced airway hyperresponsiveness in vivo and hyperresponsiveness in canine bronchi in vitro via decreased prejunctional and postjunctional inhibition (likely mediated by prostaglandin E2) and increased prejunctional excitation mediated by thromboxane A2. However, direct measurements of mediator release should be carried out to reach a firm conclusion.

Intrathyroidal autonomic nerves can directly influence hormone release from rat thyroid follicles: A study in vitro employing electrical field stimulation and intracellular microelectrodes

1987 ◽  
Vol 72 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Stephen T. Green
Keyword(s):  
Membrane Potential ◽  
Thyroid Gland ◽  
Cell Membrane ◽  
Input Resistance ◽  
Electrical Field Stimulation ◽  
Follicular Cell ◽  
Field Stimulation ◽  
Electrical Field ◽  
Rat Thyroid

1. The role of the autonomic nervous system in the control of thyroxine release from the rat thyroid gland in vitro, has been investigated using electrical field stimulation as a device to induce intrathyroidal nerves to release their neurotransmitters. 2. The effects of field stimulation on follicular cell membrane potential and input resistance have been investigated using continuous intracellular recordings from individual cells. 3. Electrical field stimulation promotes up to an eightfold increase in throxine release from the thyroid gland in vitro. This effect is blocked by the neurotoxin, tetrodotoxin. 4. Electrical field stimulation has no effect on follicular cell membrane potential or input resistance. This is consistent with the results of previous pharmacological experiments using this preparation. 5. It is concluded that electrical field stimulation induces intrathyroidal nerves to release their neurotransmitters, and that the net effect of this is to cause thyroxine release from the thyroid follicles. The existence of a directly acting secretomotor innervation to the thyroid follicle is suggested.

Lack of effect of botulinum toxin on nonadrenergic, noncholinergic inhibitory responses of the guinea pig fundus in vitro

1980 ◽  
Vol 58 (1) ◽  
pp. 88-92 ◽  
Author(s):  
M. L. Paul ◽  
M. A. Cook
Keyword(s):  
Botulinum Toxin ◽  
Guinea Pig ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Cholinergic Nerves ◽  
Electrical Field

The nonadrenergic, noncholinergic inhibitory (NAI) response of guinea pig fundic strip to electrical field stimulation was examined in the presence of botulinum toxin and tetrodotoxin. Tetrodotoxin completely abolished the NAI response while botulinum toxin did not alter it. It is concluded that the mediator of NAI responses is unlikely to be released with acetylcholine from cholinergic nerves or that such release would have to occur by a mechanism resistant to botulinum toxin.

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