Linked Life Data

20427723

Source:http://linkedlifedata.com/resource/pubmed/id/20427723

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-6-25
pubmed:abstractText
We evaluated the effects of intracerebroventricular (icv) infusion of Na(+)-rich artificial cerebrospinal fluid (aCSF), with or without the mineralocorticoid receptor (MR) blocker spironolactone, on epithelial Na(+) channel (ENaC) subunits and regulators, such as MR, serum/glucocorticoid-inducible kinase 1, neural precursor cells expressed developmentally downregulated 4-like gene, 11beta-hydroxylase, and aldosterone synthase, in brain regions of Wistar rats. The effects of icv infusion of the amiloride analog benzamil on brain tissue and CSF Na(+) concentration ([Na(+)]) were also assessed. In the choroid plexus and ependyma of the anteroventral third ventricle, ENaC subunits are present in apical and basal membranes. Na(+)-rich aCSF increased beta-ENaC mRNA and immunoreactivity in the choroid plexus and increased alpha- and beta-ENaC immunoreactivities in the ependyma. Na(+)-rich aCSF increased alpha- and beta-ENaC-gold-labeled particles in the microvilli of the choroid plexus and in basolateral membranes of the ependyma. Spironolactone only prevented the increase in beta-ENaC immunoreactivity in the choroid plexus and ependyma. In the supraoptic nucleus, paraventricular nucleus, and subfornical organ, Na(+)-rich aCSF did not affect mRNA expression levels of the studied genes. Benzamil significantly increased CSF [Na(+)] in the control, but not Na(+)-rich, aCSF group. In contrast, benzamil prevented the increase in hypothalamic tissue [Na(+)] by Na(+)-rich aCSF. These results suggest that CSF Na(+) upregulates ENaC expression in the brain epithelia, but not in the neurons of hypothalamic nuclei. ENaC in the choroid plexus and ependyma appear to contribute to regulation of Na(+) homeostasis in the brain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1522-1490
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
299
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R222-33
pubmed:meshHeading
pubmed-meshheading:20427723-Aldosterone Synthase, pubmed-meshheading:20427723-Amiloride, pubmed-meshheading:20427723-Animals, pubmed-meshheading:20427723-Biological Transport, pubmed-meshheading:20427723-Brain, pubmed-meshheading:20427723-Choroid Plexus, pubmed-meshheading:20427723-Epithelial Sodium Channel, pubmed-meshheading:20427723-Epithelium, pubmed-meshheading:20427723-Glucocorticoids, pubmed-meshheading:20427723-Hypothalamus, pubmed-meshheading:20427723-Male, pubmed-meshheading:20427723-Paraventricular Hypothalamic Nucleus, pubmed-meshheading:20427723-RNA, Messenger, pubmed-meshheading:20427723-Random Allocation, pubmed-meshheading:20427723-Rats, pubmed-meshheading:20427723-Rats, Wistar, pubmed-meshheading:20427723-Receptors, Mineralocorticoid, pubmed-meshheading:20427723-Sodium, pubmed-meshheading:20427723-Sodium, Dietary, pubmed-meshheading:20427723-Spironolactone
pubmed:year
2010
pubmed:articleTitle
Effects of central sodium on epithelial sodium channels in rat brain.
pubmed:affiliation
Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't