Linked Life Data

3030358

Source:http://linkedlifedata.com/resource/pubmed/id/3030358

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1987-5-21
pubmed:abstractText
The effects of alpha 1- and alpha 2-adrenergic agonists, viz., phenylephrine and clonidine, respectively, were studied on rat liver plasma membrane Ca++-ATPase. Phenylephrine produced a 23% inhibition of enzyme activity at 5 microM. Prazosin, an alpha 1 antagonist, completely prevented the effect of phenylephrine. Clonidine produced a comparable inhibition of Ca++-ATPase, but was not reversed by the antagonist yohimbine, suggesting a lack of functionally significant alpha 2 receptors as previously reported. The results support the role of high-affinity Ca++-ATPase in liver plasma membranes in the control of cytosolic free Ca++ levels through regulation by alpha 1-adrenergic receptors. In vitro and acute ethanol exposure produced inhibition of plasma membrane Ca++-ATPase. In addition, ethanol treatment significantly reversed the inhibitory effect of phenylephrine on Ca++-ATPase. Chronic ethanol exposure for four weeks increased Ca++-ATPase activity over control and increased enzyme activity in the presence of phenylephrine. These results demonstrate that ethanol alters the alpha-adrenergic receptor interaction with Ca++-ATPase resulting in reduced receptor regulation of cytosolic Ca++ levels. These changes may prevent the liver from maintaining Ca++ levels for second messenger functions, such as glycolysis and gluconeogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0741-8329
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-30
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:articleTitle
Effects of alcohol on alpha-adrenergic receptor regulation of calcium ATPase in liver plasma membranes.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.