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.

Neural regulation of 35SO4-macromolecule secretion from tracheal glands of ferrets

1984 ◽  
Vol 57 (2) ◽  
pp. 457-466 ◽  
Author(s):  
D. B. Borson ◽  
M. Charlin ◽  
B. D. Gold ◽  
J. A. Nadel
Keyword(s):  
Electrical Stimulation ◽  
Electrical Field Stimulation ◽  
Base Line ◽  
Field Stimulation ◽  
Cholinergic Nerves ◽  
Electrical Field ◽  
Molecular Weights ◽  
Submucosal Glands ◽  
Pharmacological Stimulation

Our goal was to determine what nervous mechanisms mediate the secretion of macromolecules from tracheal submucosal glands of ferrets. To do this, we studied the secretion of 35SO4-labeled macromolecules in vitro in response to electrical or pharmacological stimulation in the absence and presence of a specific nerve blocker and autonomic antagonists. We found that electrical field stimulation and the agonists acetylcholine, phenylephrine, terbutaline, and norepinephrine each cause secretion of radiolabeled materials. The molecular weights of the labeled materials released during base line and after electrical stimulation were greater than 1,000,000. The antagonists atropine, phentolamine, and propranolol alone prevented the responses to acetylcholine, phenylephrine, and terbutaline, respectively, without preventing responses to any other of these agonists or changing baseline secretion. Only phentolamine and propranolol together prevented the response to norepinephrine. Tetrodotoxin prevented the response to electrical stimulation but not the responses to the agonists. Each of the antagonists inhibited a significant portion of the response to electrical stimulation, but the combination of all three did not completely prevent secretion. We conclude that cholinergic nerves mediate secretion via muscarinic mechanisms, that adrenergic nerves mediate secretion via both alpha- and beta-adrenergic mechanisms, and that nonadrenergic-noncholinergic nerves mediate secretion via unidentified mechanisms.

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.

Acetylcholine release from canine isolated airway is not modulated by norepinephrine

1986 ◽  
Vol 61 (3) ◽  
pp. 1025-1030 ◽  
Author(s):  
J. G. Martin ◽  
B. Collier
Keyword(s):  
Guinea Pig ◽  
Acetylcholine Release ◽  
Electrical Field Stimulation ◽  
Output Pulse ◽  
Physiological Salt Solution ◽  
Guinea Pig Ileum ◽  
Cholinergic Nerves ◽  
Ach Release ◽  
Electrical Field ◽  
Neural Origin

We measured acetylcholine (ACh) release from canine isolated tracheal smooth muscle (TSM) and bronchial spirals using a radioenzymic assay technique. Tissue was incubated in physiological salt solution containing physostigmine (3.10(-5) M), atropine (10(-7) M), and choline (5.10(-6) M), and bath fluid was collected every 15 min for assay. There was a resting release of ACh of 209 +/- 44 pmol/g tissue (mean +/- SE) from 53 to 77 specimens of TSM. Electrical field stimulation (ES) increased ACh release, which was blocked by tetrodotoxin (10(-6) g/ml), confirming the neural origin of ACh. The ACh output during ES (2-ms pulses) at 10 Hz increased linearly from 188 +/- 50 pmol/g tissue (mean +/- SE) for a 1-min volley, to 323 +/- 57 for three volleys, and 544 +/- 128 for five volleys. The ACh output/pulse was constant during ES at 20, 15, 10, and 5 Hz, but it was significantly higher at 2 than at 5 Hz (P less than 0.005). Incubation of TSM with norepinephrine (NE, 10(-5) M) did not affect ACh output either at 2 or 10 Hz. Likewise, ACh output from bronchial spirals during ES and 2 Hz was unaffected by NE. In contrast, NE treatment of isolated guinea pig ileum reduced the ACh released by ES at 2 Hz to 40 +/- 7% (P less than 0.001) of the control ACh output. It is concluded that evoked release of ACh (output/pulse) from cholinergic nerves in canine airway is frequency dependent, as in guinea pig ileum, but that, unlike guinea pig ileum, NE does not modulate its release.

Effects of mucosal removal on guinea-pig airway smooth muscle responsiveness

1986 ◽  
Vol 70 (6) ◽  
pp. 571-575 ◽  
Author(s):  
Christopher Murlas
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
Contractile Response ◽  
Electrical Field Stimulation ◽  
Physiological Salt Solution ◽  
Induced Responses ◽  
Field Stimulation ◽  
Electrical Field ◽  
Airway Mucosa

1. The contractile response to histamine, acetylcholine (ACh), KCl or electrical field stimulation (EFS) was examined in paired tracheal rings (one of each being denuded by mucosal rubbing), which were mounted in muscle chambers filled with a continuously aerated physiological salt solution at 37°C. 2. Removal of the respiratory mucosa increased the sensitivity of airway muscle to ACh, histamine and EFS, but not to KCl. The hypersensitivity of denuded rings to histamine and EFS was greater than to ACh. Atropine reduced the histamine hypersensitivity observed. 3. Pretreating intact preparations with indomethacin augmented their responsiveness to EFS, histamine and ACh. 4. Indomethacin augmentation of histamine- and EFS-induced responses was greater in preparations without epithelium. 5. We conclude that the airway mucosa may be associated with a factor that reduces airway smooth muscle responsiveness to stimulation.

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