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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0205064,
umls-concept:C0332197,
umls-concept:C0449432,
umls-concept:C0459521,
umls-concept:C0599668,
umls-concept:C0599861,
umls-concept:C1179435,
umls-concept:C1278872,
umls-concept:C1521797,
umls-concept:C1524073,
umls-concept:C1548799,
umls-concept:C1705248
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pubmed:issue |
1
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pubmed:dateCreated |
1983-7-8
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pubmed:abstractText |
1 In rats anaesthetised with chloralose and pentobarbitone, frequency-dependent tachycardia and contraction of the ipsilateral inferior eyelid occurred when the intact right cervical sympathetic nerve was stimulated. 2 After successive doses of 5, 12.5 and 30 micrograms.kg-1 neostigmine sulphate (i.v.) a progressive reduction was seen in the tachycardias to low frequency stimulation (0.2 to 2 Hz) but either no effect, or an augmentation after 30 micrograms.kg-1, was evident at higher frequencies (up to 20 Hz). Atropine sulphate (i.v., 100 micrograms.kg-1) abolished the augmentatory effect of neostigmine on the high-frequency responses and offset partially the depressant effect of neostigmine on the responses to 0.2 and 0.5 Hz. By contrast, contractions of the eyelid were unaltered by neostigmine and atropine. 3 Reserpinised rats (8 mg.kg-1 i.p., 24 h earlier) were quite refractory to stimulation and remained so after neostigmine and atropine. 4 The effectiveness of neostigmine (enhancing responses) and atropine (inhibiting them) was demonstrated on endogenous acetylcholine (ACh) by measuring bradycardia to right efferent vagal stimulation, and on exogenous ACh by measuring inferior eyelid retraction in both reserpinised and control rats. These groups were equally sensitive to either ACh or noradrenaline and cocaine potentiated the tachycardia to noradrenaline in both groups. 5 Propranolol reduced the tachycardia and phentolamine the eyelid contraction induced by sympathetic nerve stimulation. 6 The findings offer no support to a theory implying an obligatory cholinergic-link in noradrenergic transmission.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0144-1795
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
13-20
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:6304103-Animals,
pubmed-meshheading:6304103-Drug Interactions,
pubmed-meshheading:6304103-Electric Stimulation,
pubmed-meshheading:6304103-Female,
pubmed-meshheading:6304103-Neostigmine,
pubmed-meshheading:6304103-Norepinephrine,
pubmed-meshheading:6304103-Parasympathetic Nervous System,
pubmed-meshheading:6304103-Rats,
pubmed-meshheading:6304103-Reserpine,
pubmed-meshheading:6304103-Sympathetic Nervous System,
pubmed-meshheading:6304103-Synaptic Transmission,
pubmed-meshheading:6304103-Vagus Nerve
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pubmed:year |
1983
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pubmed:articleTitle |
Absence of a cholinergic component in noradrenergic transmission in the cervical sympathetic nerve of the rat.
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pubmed:publicationType |
Journal Article
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