Linked Life Data

20054292

Source:http://linkedlifedata.com/resource/pubmed/id/20054292

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-2-26
pubmed:abstractText
Dietary sodium and potassium contribute to the control of the blood pressure. Endothelial cells are targets for aldosterone, which activates the apically located epithelial sodium channels. The activity of these channels is negatively correlated with the release of nitric oxide (NO) and determines endothelial function. A mediating factor between channel activity and NO release is the mechanical stiffness of the cell's plasma membrane, including the submembranous actin network (the cell's 'shell'). Changes in plasma sodium and potassium, within the physiological range, regulate the viscosity of this shell and thus control the shear-stress-dependent activity of the endothelial NO synthase located in the shell's 'pockets' (caveolae). High plasma sodium gelates the shell of the endothelial cell, whereas the shell is fluidized by high potassium. Accordingly, this concept envisages that communications between extracellular ions and intracellular enzymes occur at the plasma membrane barrier, whereas 90% of the total cell mass remains uninvolved in these changes. Endothelial cells are highly sensitive to extracellular sodium and potassium. This sensitivity may serve as a physiological feedback mechanism to regulate local blood flow. It may also have pathophysiological relevance when sodium/potassium homeostasis is disturbed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1523-1755
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
490-4
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Endothelial cells as vascular salt sensors.
pubmed:affiliation
Medical Faculty, Institute of Physiology II, University of Münster, 48149 Münster, Germany. oberlei@uni-muenster.de
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't