Distribution and function of enteric GAL-IR nerves in dogs: comparison with VIP

1989 ◽  
Vol 256 (5) ◽  
pp. G884-G896 ◽  
Author(s):  
T. Gonda ◽  
E. E. Daniel ◽  
T. J. McDonald ◽  
J. E. Fox ◽  
B. D. Brooks ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Vasoactive Intestinal Polypeptide ◽  
Myenteric Plexus ◽  
Low Doses ◽  
Field Stimulation ◽  
And Function ◽  
Higher Doses ◽  
Stimulation Of

The distribution of nerves containing galanin-immunoreactive (GAL-IR) material was compared to the distribution of neurons containing vasoactive intestinal polypeptide (VIP) immunoreactivity in the canine gastrointestinal tract. The actions of intra-arterially administered galanin and VIP on motility in the gastric antrum and corpus and the intestines were also studied. All sphincter muscles contained galanin- and VIP-immunoreactive nerve profiles. VIP-immunoreactive nerve profiles were present in all layers of the stomach, small intestine, and colon. GAL-IR nerve somata were common in the submucous plexus of ileum and colon and in the myenteric plexus of the terminal antrum, as were nerve processes in various layers. In the small intestine, galanin inhibited contractile responses to field stimulation of intrinsic nerves and also reduced the contractions after nerve blockade with tetrodotoxin (TTX). VIP often enhanced field-stimulated contractions at low doses but inhibited these and the contractions after TTX at higher doses. In the stomach and colon, both peptides inhibited responses to field stimulation; whether these effects were due to actions on smooth muscle was not tested. The distribution and actions of galanin in gut are consistent with the hypothesis that it acts at smooth muscle sites and possibly at prejunctional sites.

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.

Exogenous opiates: their local mechanisms of action in the canine small intestine and stomach

1987 ◽  
Vol 253 (2) ◽  
pp. G179-G188 ◽  
Author(s):  
J. E. Fox ◽  
E. E. Daniel
Keyword(s):  
Small Intestine ◽  
Mechanisms Of Action ◽  
Low Doses ◽  
Field Stimulation ◽  
Direct Stimulation ◽  
Distal Stomach ◽  
Phasic Activity ◽  
Release Of Acetylcholine ◽  
Relative Potencies ◽  
Stimulation Of

Methionine-enkephalin (Met-Enk) and dynorphin were injected intra-arterially into the distal stomach and small intestine of the anesthetized dog during quiescence and phasic activity initiated by field stimulation or intra-arterially administered motilin. The effects of morphine, [D-Ala2, N-Me-Phe4, Met(O)5-ol]enkephalin (Met-ol), and [D-Ala2, D-Leu5]enkephalin (DADLE) were also examined. Opiates had no effect on the quiescent stomach but produced inhibition of phasic contractions (potencies: dynorphin greater than Met-Enk greater than Met-ol greater than DADLE greater than morphine). In the quiescent small intestine, low doses of each opiate, except dynorphin, produced excitation (potencies: Met-Enk congruent to Met-ol congruent to DADLE greater than morphine). Excitation apparently occurred via release of acetylcholine and a partially naloxone-sensitive direct stimulation of smooth muscle. During phasic activity all opiates produced inhibition of phasic muscular contractions (relative potencies as in the stomach). Inhibition by dynorphin in both the stomach and small intestine was shown to occur via naloxone-sensitive inhibition of release of acetylcholine from nerves. Thus inhibition by opiates appears common to the stomach and small intestine, and excitation is a function of opiate action only in the small intestine. Dynorphin may be a natural neuropeptide causing inhibition, and Met-Enk may be a natural neuropeptide causing excitation.

Intracellular electrical activity of muscularis mucosae of the dog stomach

1985 ◽  
Vol 249 (2) ◽  
pp. G256-G263 ◽  
Author(s):  
K. G. Morgan ◽  
F. Angel ◽  
P. F. Schmalz ◽  
J. H. Szurszewski
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Activity ◽  
Vasoactive Intestinal Polypeptide ◽  
Mechanical Activity ◽  
Field Stimulation ◽  
Muscularis Mucosae ◽  
Spike Potential ◽  
Stimulation Of ◽  
Intestinal Polypeptide

Mechanical and intracellular electrical activity was recorded simultaneously in vitro from smooth muscle of the muscularis mucosae of the canine antrum. The intracellularly recorded membrane potential averaged -51 +/- 1.4 mV (mean +/- SE). Spontaneous electrical activity consisted of spike-shaped potentials that were 20–40 mV in amplitude. The rate of rise of the spike potential was slow (less than 0.2 V/s) and the half-time duration was long (0.5-5.0 s). Phasic contractions were often but not always coupled with spike potentials. Ion substitution studies suggested that the spike potential had a greater dependence on Na+ than on Ca2+. Field stimulation of intramural nerves hyperpolarized the membrane potential and abolished spikes or reduced their amplitude and frequency. These changes were associated with a reduction in tone and phasic contractile activity. The response to stimulation of inhibitory nerves was mimicked by epinephrine, neurotensin, and vasoactive intestinal polypeptide. The resistance to adrenergic blocking agents ruled out the possibility of norepinephrine as the transmitter. The tetrodotoxin sensitivity of the response to neurotensin suggests that neurotensin acts indirectly through the inhibitory nerves. Mimicry between the action of applied vasoactive intestinal polypeptide (VIP) and field stimulation provides support for the hypothesis that VIP may be an inhibitory neurotransmitter. These studies indicate that smooth muscle in the canine gastric muscularis mucosae generates spontaneous electrical and mechanical activity and receives a noncholinergic, nonadrenergic inhibitory innervation.

The effects of substance P and met-enkephalin in dog ileum

1982 ◽  
Vol 60 (6) ◽  
pp. 830-840 ◽  
Author(s):  
E. E. Daniel ◽  
T. Gonda ◽  
T. Domoto ◽  
M. Oki ◽  
N. Yanaihara
Keyword(s):  
Smooth Muscle ◽  
Substance P ◽  
Local Field ◽  
Tonic Contraction ◽  
Low Doses ◽  
Field Stimulation ◽  
Cholinergic Nerves ◽  
Higher Doses ◽  
Postganglionic Neurones

Substance P initiated tonic contraction of dog ileum when administered in doses from 1 pg to 20 μg intraarterially (ED50 = 67 ng). Low doses acted to excite cholinergic postganglionic neurones since atropine or tetrodotoxin (TTX) increased the ED50 of substance P about 25-fold, while hexamethonium and local field stimulation had only a small effect to increase the ED50. Also atropine and tetrodotoxin effects were not additive. Higher doses apparently acted to stimulate smooth muscle directly, but no evidence was obtained that local field stimulation could release substance P to act on smooth muscle. Substance P tachyphylaxis prevented substance P actions on cholinergic nerves, but it did not affect responses to intraarterial acetylcholine or block distal inhibition from proximal distention or field stimulation. Met-enkephalin given intraarterially, was also excitatory in doses from 1 ng to 20 μg; the amplitude of tonic and phasic contractions produced was significantly decreased by TTX and atropine but was not diminished by hexamethonium or substance P tachyphylaxis. Partial tachyphylaxis to met-enkephalin was produced without affecting the ED50 for substance P. We conclude that substance P acts in small amounts on receptors in myenteric nerves to release acetylcholine by a mechanism, presumably involving postganglionic cholinergic nerves, while met-enkephalin also apparently may act at least in part through a similar TTX- and atropine-sensitive mechanism. These peptides also caused activation of other receptors, probably on smooth muscle by noncholinergic, TTX-insensitive mechanisms. Also the receptors for each peptide which are located on nerves were distinct and independent since tachyphylaxis could be produced to each without affecting the response to the other.not available

Activation of endogenous excitatory opiate pathways in canine small intestine by field stimulation and motilin

1987 ◽  
Vol 253 (2) ◽  
pp. G189-G194 ◽  
Author(s):  
J. E. Fox ◽  
E. E. Daniel
Keyword(s):  
Small Intestine ◽  
Field Stimulation ◽  
Methionine Enkephalin ◽  
Intrinsic Nerves ◽  
Higher Doses ◽  
Excitatory Transmitter ◽  
Stimulation Of

Field stimulation of intrinsic nerves (40 V, 0.5 ms, 1-5 pps for 3-10 min) or intraarterial administration of motilin (10(-11)-10(-8 mol) caused contractions of the canine small intestine that were partially resistant to atropine and abolished by tetrodotoxin. Naloxone (10 micrograms ia or 200 micrograms/kg iv) in selective doses (10(-10)-10(-9) mol) that left responses to intra-arterial acetylcholine unaffected reduced responses to field stimulation or motilin in the ileum in the absence of atropine or residual responses in the presence of atropine. Results in the jejunum were similar except that selective doses of naloxone (10 micrograms ia or 200 micrograms/kg iv) increased the sensitivity to motilin in the absence of atropine. Higher doses of naloxone decreased these responses. In common with naloxone, tachyphylaxis to methionine-enkephalin (Met-Enk) reduced the responses to field stimulation or motilin before or after atropine but did not affect the responses to acetylcholine before or the responses to field stimulation of muscle after atropine. These findings are consistent with the hypothesis that Met-Enk may be a noncholinergic, excitatory transmitter released by field stimulation of nerves or intra-arterial motilin in the canine intestine.

Structural and functional study of control of canine tracheal smooth muscle

1980 ◽  
Vol 238 (1) ◽  
pp. C27-C33 ◽  
Author(s):  
M. S. Kannan ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Electrical Field Stimulation ◽  
Sympathetic Nerves ◽  
Tracheal Smooth Muscle ◽  
Functional Study ◽  
Field Stimulation ◽  
Electron Microscopic ◽  
Microscopic Studies ◽  
Stimulation Of

The structural bases for myogenic and neurogenic control of canine tracheal smooth muscle were studied. At optimum lengths, strips of muscle showed insignificant neurogenic or myogenic tone. Atropine and/or tetrodotoxin blocked the contractile responses elicited on electrical field stimulation of intrinsic nerves. After raising the tone with tetraethylammonium ion and in the presence of atropine, field stimulation of nerves caused a relaxation, a major component of which was blocked by propranolol and/or tetrodotoxin, suggesting an effect mediated through interaction of mediator released from sympathetic nerves with beta-adrenergic receptors. Electron microscopic studies revealed gap junctions between extensions of smooth-muscle cells and a sparse innervation. The axonal varicosities, corresponding to cholinergic (predominantly) and adrenergic (occasionally) nerves, were seen predominantly in the clefts between cell bundles. The physiological responses were compared with the morphological features. Although this muscle exhibits multiunit behavior in vitro, implying that nerves initiate the coordinate activity, its ultrastructural features suggest a potential for single-unit behavior.

Expression and function of 5-hydroxytryptamine 4 receptors in smooth muscle preparations from the duodenum, ileum, and pelvic flexure of horses without gastrointestinal tract disease

2010 ◽  
Vol 71 (12) ◽  
pp. 1432-1442 ◽  
Author(s):  
Andrea S. Prause ◽  
Christophe T. Guionaud ◽  
Michael H. Stoffel ◽  
Christopher J. Portier ◽  
Meike Mevissen
Keyword(s):  
Smooth Muscle ◽  
Gastrointestinal Tract ◽  
Tract Disease ◽  
And Function

Temperature dependence of responses of esophageal smooth muscle to electrical field stimulation.

1977 ◽  
Vol 232 (4) ◽  
pp. E432
Author(s):  
D J De Carle ◽  
A C Szabo ◽  
J Christensen
Keyword(s):  
Smooth Muscle ◽  
Temperature Dependence ◽  
Electrical Field Stimulation ◽  
Ringer Solution ◽  
Current Strength ◽  
Field Stimulation ◽  
Electrical Field ◽  
Linear Decline ◽  
Temperature Amplitude ◽  
Stimulation Of

Strips of smooth muscle, cut transversely from the smooth-muscle segment of opossum esophagus, were superfused with oxygenated Krebs-Ringer solution at 37 degrees C in a system that allowed electrical field stimulation of the intrinsic nerves. Three-to-five-second trains of rectangular pulses (0.5 ms long at 10 Hz) were delivered at 30-s intervals at supramaximal maximal current strength. In strips from the esophageal body, each train resulted in a twitch which followed after the end of train with a particular latency, the off-response. Strips from the esophagogastric sphincter relaxed during the train. Temperature was varied above and below 37 degrees C to observe the temperature dependence of the responses. Latency of the off-response varied exponentially with temperature. Amplitude of the off-response showed a linear decline with changes in temperature, both above and below 35 degrees C, the zero-intercepts being 19.6 and 42.3 degrees C, respectively. Amplitude of relaxation of strips from the junction varied little between 20 and 37 degree C but declined sharply beyond those limits, the zero-intercepts being 14.2 and 42 degrees C, respectively.

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