Linked Life Data

9074969

Source:http://linkedlifedata.com/resource/pubmed/id/9074969

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-6-27
pubmed:abstractText
From the 1930s into the 1970s, the role of acetylcholine (ACh) in the carotid body's chemotransduction of hypoxia was debated. Since the late 1970s, the issue has been pursued only intermittently or not at all. The purpose of this study was to test again with a new preparation the hypothesis that ACh is an excitatory neurotransmitter in the cat carotid body's chemotransduction of hypoxia. We tested the effect of the specific nicotinic blocker mecamylamine and the muscarinic blocker of all five muscarinic receptors, atropine. We further tested the effects of M1 and M2 muscarinic-receptor blockers. The carotid body region was selectively perfused with hypoxic Krebs-Ringer bicarbonate (KRB) solutions that were blocker free or contained varying doses of the blockers. Both mecamylamine and atropine reduced the response to hypoxic KRB in a dose-related manner. The M2 muscarinic-receptor blockers gallamine and AFDX 116 increased the response to hypoxic KRB, whereas the M1 muscarinic-receptor blocker pirenzepine reduced the response to hypoxic KRB. These data are consistent with an excitatory role for ACh in the carotid body chemotransduction of hypoxia in the cat.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
819-27
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Further cholinergic aspects of carotid body chemotransduction of hypoxia in cats.
pubmed:affiliation
Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.