Linked Life Data

1940019

Source:http://linkedlifedata.com/resource/pubmed/id/1940019

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-11-26
pubmed:abstractText
The effects of chronic acrylamide treatment on the autonomic nervous system were investigated by histochemical and pharmacological studies. Histochemical studies showed that acrylamide caused different degrees of damage to different nerve fibre types: calcitonin gene-related peptide (CGRP)-immunoreactive (IR) nerves showed the greatest reduction in intensity and number; noradrenaline (NA)-containing nerves were somewhat less affected; substance P (SP)-IR nerves were reduced in number, but this was not significant. The profiles of SP- and particularly of CGRP-IR nerves from treated animals were noticeably different to those from the control group, being flattened and irregular. Periarterial nerve stimulation (4-32 Hz) of the isolated rat mesenteric arterial bed preparation at basal tone elicited frequency-dependent vasoconstrictor responses. The magnitude of these responses was significantly reduced at higher frequencies in acrylamide-treated animals. In preparations with tone raised by the addition of methoxamine (10(-5) M), and in the presence of guanethidine (5 x 10(-6) M), periarterial nerve stimulation elicited vasodilator responses. These responses, which result from stimulation of sensory nerves, were greatly reduced in acrylamide-treated animals. There was a tendency for mesenteric beds from acrylamide-treated animals to show increased vasoconstrictor responses to doses of exogenous NA, although this was not significant. Responses to exogenous adenosine 5'-triphosphate (a cotransmitter with NA from sympathetic nerves) were not affected. In the raised-tone preparation, vasodilator responses to exogenous CGRP (the principal vasodilator sensory transmitter of rat mesenteric arteries) were not affected by acrylamide treatment. Hence, it is unlikely that the reduced responses to nerve stimulation were due to defects in the postjunctional receptors for the principal transmitters of sympathetic and sensory-motor nerves. There was no difference in the ability of mesenteric beds from control and treated animals to vasodilate in response to acetylcholine or sodium nitroprusside, or to vasoconstrict in response to potassium chloride, indicating normal smooth muscle and endothelial responses. These results suggest that chronic acrylamide treatment produces peripheral autonomic neuropathy of rat mesenteric vessels, manifested as a dysfunction of sympathetic and sensory-motor nerves. Furthermore, the graded destruction of nerve types, such that damage occurred in the order: CGRP-IR greater than NA greater than SP-IR, indicated a differential sensitivity of different nerves to this toxin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0165-1838
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
77-87
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Acrylamide-induced autonomic neuropathy of rat mesenteric vessels: histological and pharmacological studies.
pubmed:affiliation
Department of Anatomy and Developmental Biology, University College, London, U.K.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't