Linked Life Data

1975083

Source:http://linkedlifedata.com/resource/pubmed/id/1975083

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1990-9-27
pubmed:abstractText
The mechanisms by which activation of alpha 2-adrenoceptors inhibits insulin release are still incompletely understood. This study, performed with isolated mouse islets, identifies a possible role of Na+ in this inhibition. Regardless of the stimulus used to induce insulin release, the inhibitory effect of low concentrations of clonidine (0.01-0.1 microM) was markedly smaller in the absence of Na+ (with choline or lithium as substitute) than in its presence. The effectiveness of a high concentration of clonidine (1 microM) was, however, not affected by Na+ omission. The results indicate either that Na+ omission indirectly counteracts an effect of clonidine (e.g. on a membrane permeability or on Ca2+ handling), or that Na+ is directly involved in a cellular process (e.g. a Na+ current or the Na+/H+ exchange) controlled by alpha 2-adrenoceptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
299-305
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
The influence of sodium omission on alpha 2-adrenergic inhibition of insulin release by mouse islets.
pubmed:affiliation
Unité de Diabétologie et Nutrition, University of Louvain, Faculty of Medicine, Brussels, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't