Regulation of intestinal goblet cell secretion. IV. Electrical field stimulation in vitro

1984 ◽  
Vol 247 (6) ◽  
pp. G682-G687 ◽  
Author(s):  
T. E. Phillips ◽  
T. H. Phillips ◽  
M. R. Neutra
Keyword(s):  
Cholinergic Neurons ◽  
Electrical Field Stimulation ◽  
Goblet Cells ◽  
Mucus Secretion ◽  
Enteric Neurons ◽  
Field Stimulation ◽  
Cell Secretion ◽  
Electrical Field ◽  
Ussing Chambers

To determine whether transmitters released from enteric neurons can elicit secretion from goblet cells, full-thickness sheets of adult rat distal ileum or descending colon were mounted in modified Ussing chambers, and mucus secretion was assessed morphologically after electrical field stimulation (EFS). Square-wave pulses (56 V, 2 ms duration) were delivered at 10 Hz for 5 min. Goblet cells in colonic crypts, but not those on the mucosal surface, secreted mucus in response to EFS. This secretion was at least in part atropine insensitive, indicating a noncholinergic mechanism. In the ileum goblet cells located in the crypts, but not on villi, secreted mucus when tissue was mounted in the chamber, even in the absence of EFS. This “unelicited” secretion did not occur in unmounted control tissue in vitro, and it could be prevented by preincubating ileal tissue in 1 microM tetrodotoxin (TTX) or 10 microM atropine for 15 min before mounting. Furthermore, following preincubation with either TTX or atropine, EFS' failed to elicit secretion. Incubation of unmounted tissue with TTX, however, did not block the secretory response of crypt goblet cells to 20 microM carbachol. Thus, intrinsic cholinergic neurons may be sxtimulated during the mounting of the ileum in the chamber. Taken together, these data demonstrate that mucus secretion from crypt goblet cells may be regulated by cholinergic (in ileum and perhaps colon) and noncholinergic (in colon) elements of the enteric nervous system.

Treatment of gastric ulcers and diarrhea with the Amazonian herbal medicine sangre de grado

2000 ◽  
Vol 279 (1) ◽  
pp. G192-G200 ◽  
Author(s):  
Mark J. S. Miller ◽  
Wallace K. MacNaughton ◽  
Xiao-Jing Zhang ◽  
Jane H. Thompson ◽  
Randi M. Charbonnet ◽  
...  
Keyword(s):  
Herbal Medicine ◽  
Cost Effective ◽  
Electrical Field Stimulation ◽  
Skin Lesions ◽  
Gastric Ulcers ◽  
Myeloperoxidase Activity ◽  
Field Stimulation ◽  
Electrical Field ◽  
Ussing Chambers ◽  
Cost Effective Treatment

Sangre de grado is an Amazonian herbal medicine used to facilitate the healing of gastric ulcers and to treat gastritis, diarrhea, skin lesions, and insect stings. This study was designed to evaluate the gastrointestinal applications. Gastric ulcers were induced in rats by brief serosal exposure of the fundus to acetic acid (80%). Sangre de grado was administered in drinking water at 1:1,000 and 1:10,000 dilutions from the postoperative period to day 7. Guinea pig ileum secretory responses to capsaicin, electrical field stimulation, and the neurokinin-1 (NK-1) agonist [Sar9,Met(O2)11]substance P were examined in Ussing chambers. Sangre de grado facilitated the healing of experimental gastric ulcer, reducing myeloperoxidase activity, ulcer size, and bacterial content of the ulcer. The expression of proinflammatory genes tumor necrosis factor-α, inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, IL-6, and cyclooxygenase-2 was upregulated by ulcer induction but reduced by sangre de grado treatment, particularly iNOS and IL-6. In Ussing chambers, sangre de grado impaired the secretory response to capsaicin but not to electrical field stimulation or the NK-1 agonist. We conclude that sangre de grado is a potent, cost-effective treatment for gastrointestinal ulcers and distress via antimicrobial, anti-inflammatory, and sensory afferent-dependent actions.

Regulation of intestinal goblet cell secretion. III. Isolated intestinal epithelium

1984 ◽  
Vol 247 (6) ◽  
pp. G674-G681 ◽  
Author(s):  
T. E. Phillips ◽  
T. H. Phillips ◽  
M. R. Neutra
Keyword(s):  
Intestinal Epithelium ◽  
Direct Action ◽  
Intercellular Junctions ◽  
Goblet Cells ◽  
Mucus Secretion ◽  
Cell Secretion ◽  
Adult Rats ◽  
Compound Exocytosis

Cholinergic secretagogues evoke mucus secretion from goblet cells in the crypts of small and large intestinal mucosa in vivo and in organ culture. It was not known whether this response reflected a direct action on epithelial cell receptors or an indirect effect involving intermediate neurons of the enteric nervous system. To resolve this, carbachol was applied to isolated intestinal epithelium maintained in vitro. Intact sheets of epithelium, measuring 10–200 mm2, were isolated from the ileum and colon of adult rats following short intravascular perfusion with 30 mM EDTA. The isolated epithelia lacked a basal lamina and cytoplasmic blebs formed on the basal cell surfaces, but cell ultrastructure was normal and intercellular junctions were intact. Autoradiography revealed that both goblet and columnar cells continued to incorporate [3H]glucosamine into nascent secretory macromolecules for at least 45 min after isolation. When exposed to 20 microM carbachol for 5 min, crypt goblet cells discharged their stored mucin granules by compound exocytosis, whereas goblet cells in portions of the epithelium derived from villi or mucosal surfaces were unresponsive. We conclude that cholinergic secretagogues act directly on crypt epithelial cells to elicit mucus secretion.

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.

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.

Substance P enhances electrical field stimulation-induced mast cell degranulation in rat trachea

1996 ◽  
Vol 270 (6) ◽  
pp. L985-L991 ◽  
Author(s):  
X. Y. Hua ◽  
S. M. Back ◽  
E. K. Tam
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Substance P ◽  
Electrical Field Stimulation ◽  
Mast Cell Degranulation ◽  
Facilitatory Effect ◽  
Neurokinin A ◽  
Field Stimulation ◽  
Cell Secretion ◽  
Electrical Field

We previously demonstrated in an ex vivo rat tracheal model that chymotryptic activity is an index of mast cell degranulation and that substance P (SP) and electrical field stimulation (EFS) synergistically degranulate mucosal and connective tissue mast cells. In the current study, we found that the facilitatory effect of SP was apparent at concentrations as low as 10(-9) M. This effect was mimicked by 10(-7) M neurokinin A or by 10(-6) M capsaicin and was blocked by the NK1 receptor antagonist CP-96,345. SP + EFS-induced mast cell secretion was significantly attenuated by 10(-6) M tetrodotoxin. The response was also attenuated in tracheas from rats in which sensory nerves had been depleted by systemic pretreatment with capsaicin or in which sympathetic nerves had been depleted by systemic pretreatment with 6-hydroxy-dopamine. Atropine (10(-6) M) or indomethacin (10(-5) M) also attenuated SP + EFS-induced mast cell secretion. Our findings suggest the importance of a sensitizing rather than a direct stimulating effect of SP on mast cell degranulation. SP may increase the sensitivity of mast cells to EFS-discharged mediators or facilitate the release of mast cell-stimulating mediators from autonomic nerves.

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.

Allergen-induced airway hyperresponsiveness in Brown-Norway rat: role of parasympathetic mechanisms

1993 ◽  
Vol 75 (1) ◽  
pp. 279-284 ◽  
Author(s):  
W. Elwood ◽  
T. Sakamoto ◽  
P. J. Barnes ◽  
K. F. Chung
Keyword(s):  
Airway Hyperresponsiveness ◽  
Allergen Challenge ◽  
Electrical Field Stimulation ◽  
Airway Responsiveness ◽  
Brown Norway ◽  
Field Stimulation ◽  
Electrical Field ◽  
Norway Rat

Enhanced parasympathetic mechanisms may contribute to airway hyperresponsiveness. The present study examined whether the in vivo increase in airway responsiveness seen 18–24 h after either a single or chronic aerosolized allergen challenge protocol in actively sensitized Brown-Norway rats was due to altered parasympathetic mechanisms. The roles of central and reflex vagal mechanisms were studied by performing bilateral cervical vagotomy before measurement of airway responsiveness. Bilateral vagotomy failed to reduce the increase in airway responsiveness after either a single or chronic allergen challenge. The roles of increased neural release of acetylcholine (ACh) and increased end organ responsiveness were studied in vitro. The isometric responses of tracheal and bronchial strips to both electrical field stimulation and exogenously applied ACh from rats exposed both to single and chronic allergen challenges were compared with those from saline-exposed rats. The responses to electrical field stimulation and to exogenous ACh were not significantly enhanced 18–24 h after either protocol. We conclude that the airway hyperresponsiveness observed in this allergic rat model is not mediated through an enhancement of parasympathetic mechanisms.

Effect of hyperoxia on substance P expression and airway reactivity in the developing lung

1997 ◽  
Vol 273 (1) ◽  
pp. L40-L45 ◽  
Author(s):  
F. H. Agani ◽  
N. T. Kuo ◽  
C. H. Chang ◽  
I. A. Dreshaj ◽  
C. F. Farver ◽  
...  
Keyword(s):  
Substance P ◽  
Electrical Field Stimulation ◽  
Postnatal Life ◽  
Field Stimulation ◽  
Nk1 Receptor ◽  
Cholinergic Stimulation ◽  
Airway Reactivity ◽  
Electrical Field ◽  
Contractile Responses

This study was undertaken to characterize changes in the tachykinin system induced by hyperoxic exposure and the potential effects on airway contractile responses. We exposed 7-day-old rat pups to either room air or hyperoxia (> 95% O2) for 7 days to assess pulmonary beta-preprotachykinin (beta-PPT) gene expression, substance P (SP) levels, and airway contractile responses to cholinergic stimulation before and after neurokinin-1 (NK1) receptor blockade. Lung beta-PPT mRNA expression, lung and tracheal SP levels, and contractile responses to exogenous acetylcholine and electrical field stimulation were measured in vitro in normoxia- and hyperoxia-exposed tracheal cylinders. Hyperoxia caused a 1.1- to 2.6-fold increase in steady-state lung beta-PPT mRNA and a 50 and 32% increase in SP levels of lung and trachea, respectively. In response to cholinergic stimulation, maximal contractile force (Emax) of hyperoxia exposed tracheal muscle was significantly higher than for normoxic controls. Addition of the SP (NK1) receptor blocker CP-99994 (10 microM) decreased sensitivity to electrical field stimulation in both hyperoxic and normoxic trachea without a significant decline in Emax. These data provide evidence for both increased SP production and enhanced maximal contractile responses of hyperoxia-exposed neonatal trachea to cholinergic stimulation. The tachykinin peptide SP does not, however, appear to play a major role in the enhanced airway reactivity associated with hyperoxic lung injury during early postnatal life.

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