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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1989-10-18
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pubmed:abstractText |
The guinea-pig ileum longitudinal muscle-myenteric plexus preparation, preincubated with 3H-choline or 3H-noradrenaline, was mounted in an organ bath and superfused with Tyrode's solution. Alaproclate (2-(4-chlorophenyl)-1,1-dimethyl 2-aminopropanoate) (0.01-0.5 mmol/l) reduced (IC50 = 0.1 mmol/l) and at about 0.5 mmol/l completely blocked the electrically evoked 3H-acetylcholine secretion. The depressing effect of alaproclate (0.2 mmol/l) was not counteracted by atropine (0.01, 1 or 10 mumol/l), hexamethonium (0.1 mmol/l), phentolamine (1 mumol/l) yohimbine (1 mumol/l), haloperidol (1 mumol/l), 8-phenyltheophylline (10 mumol/l), cyproheptadine (1 mumol/l), metitepine (1 mumol/l), bicuculline (10 mumol/l), picrotoxinin (0.1 mmol/l), forskolin (25 mumol/l), 3-isobutyl-1-methylxanthine (5 mmol/l), nifedipine (1 mumol/l), verapamil (1 mumol/l), dilitiazem (1 mumol/l), high calcium (6 mmol/l), high potassium (10 or 15 mmol/l), tetraethylammonium (2 mmol/l), 4-aminopyridine (0.5 mmol/l), apamin (0.5 mumol/l), barium (0.5 mmol/l) or quinine (0.1 mmol/l). Among the potassium channel blockers tested only quinine (at 0.5 or 1 mmol/l), in the same manner as lidocaine, reduced the evoked secretion of 3H-acetylcholine. The results are in agreement with the hypothesis that the effect of alaproclate on the evoked 3H-acetylcholine secretion is not mediated by a neurotransmitter receptor, or a potassium channel sensitive to tetraethylammonium, 4-aminopyridine, apamin, or barium or quinine, but is due to a local anaesthetic effect. In contrast to the evoked secretion, the spontaneous release of 3H-acetylcholine was enhanced by high concentrations of alaproclate (0.4-1 mmol/l). The mechanism underlying the effect of alaproclate on the spontaneous release remains to be established. Alaproclate (0.25 or 0.5 mmol/l) also enhanced the spontaneous release and reduced the electrically evoked 3H-noradrenaline secretion.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Alanine,
http://linkedlifedata.com/resource/pubmed/chemical/Antidepressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Lidocaine,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium,
http://linkedlifedata.com/resource/pubmed/chemical/alaproclate
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0901-9928
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
65
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25-32
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:2780505-Acetylcholine,
pubmed-meshheading:2780505-Alanine,
pubmed-meshheading:2780505-Animals,
pubmed-meshheading:2780505-Antidepressive Agents,
pubmed-meshheading:2780505-Cholinergic Fibers,
pubmed-meshheading:2780505-Electric Stimulation,
pubmed-meshheading:2780505-Guinea Pigs,
pubmed-meshheading:2780505-Ileum,
pubmed-meshheading:2780505-Lidocaine,
pubmed-meshheading:2780505-Myenteric Plexus,
pubmed-meshheading:2780505-Norepinephrine,
pubmed-meshheading:2780505-Potassium Channels,
pubmed-meshheading:2780505-Sympathetic Nervous System,
pubmed-meshheading:2780505-Tritium
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pubmed:year |
1989
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pubmed:articleTitle |
Effects of alaproclate, potassium channel blockers, and lidocaine on the release of 3H-acetylcholine from the guinea-pig ileum myenteric plexus.
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pubmed:affiliation |
Division of Experimental Medicine, Swedish Defence Research Establishment, Umeå.
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pubmed:publicationType |
Journal Article
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