Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1977-2-16
pubmed:abstractText
In isolated bovine adrenals perfused with Locke solution in a retrograde fashion we investigated the effects of halothane on the catecholamine release evoked by various secretagogues. 1. The catecholamine release induced by activation of the nicotinic receptors on the chromaffin cells with 1,1-dimethyl-4-phenylpiperazinium was almost completely inhibited (by about 90%) by 1.4 X 10(-3) M halothane. 2. It was shown by means of cumulative concentration-response curves of acetylcholine for its stimulating effect on catecholamine release (pD2 = 4.04) that halothane was a non-competitive antagonist (pD'2 = 3.17). 3. Halothane (1.4 X 10(-3) and 4.3 X 10(-3) M) did not decrease the catecholamine secretion in response to pilocarpine or histamine. 4. The 5-hydroxytryptamine-induced catecholamine release was not impaired by 1.4 X 10(-3) M halothane, but was significantly inhibited (by 44%) by 4.3 X 10(-3) M halothane. 5. At 1.4 X 10(-3) M halothane the catecholamine release induced by gamma-aminobutyric acid (GABA) was inhibited by 40%. 4.3 X 10(-3) M halothane completely blocked the secretion induced by GABA. 6. The catecholamine secretion in response to 56 mM KCl or to introduction of CaCl2 after perfusion with Locke solution deficient in CaCl2 was not reduced by halothane (1.4 X 10(-3) and 1.4 X 10(-2) M). 7. Halothane (1.4 X 10(-3) M) did not inhibit the catecholamine release evoked by acetaldehyde or tyramine from glands perfused with Ca2+ -free Locke solution throughout the experiments. It is concluded that the site of action of halothane is the cell membrane of the chromaffin cell. The anaesthetic does not impair the permeability of the membrane to calcium ions. Halothane may cause a conformational change of membrane proteins, particularly of the nicotinic receptor (and at higher concentrations of GABA and 5-hydroxytryptamine receptors); thus, stimulation may be prevented by an inhibition of agonist-receptor interaction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Acetaldehyde, http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Calcium Chloride, http://linkedlifedata.com/resource/pubmed/chemical/Catecholamines, http://linkedlifedata.com/resource/pubmed/chemical/Dimethylphenylpiperazinium Iodide, http://linkedlifedata.com/resource/pubmed/chemical/Halothane, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nicotinic, http://linkedlifedata.com/resource/pubmed/chemical/Serotonin, http://linkedlifedata.com/resource/pubmed/chemical/Tyramine, http://linkedlifedata.com/resource/pubmed/chemical/gamma-Aminobutyric Acid
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0028-1298
pubmed:author
pubmed:issnType
Print
pubmed:volume
294
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
239-49
pubmed:dateRevised
2010-3-12
pubmed:meshHeading
pubmed:year
1976
pubmed:articleTitle
Inhibition of catecholamine release from the adrenal medulla by halothane. Site and mechanism of action.
pubmed:publicationType
Journal Article