Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-12-4
pubmed:abstractText
Nitric oxide (NO) is an important gas mediator in the signal transduction cascade regulating osmotic function in the hypothalamo-neurohypophysial system. We previously found that increased nitric oxide synthase (NOS) activity in the supraoptic nuclei (SON) and neural lobe following osmotic stimulation and NO could regulate the expression of Ca(2+)-activated K(+) channel (BK channels) protein in the magnocellular system during dehydration. The aim of the current study is to examine the role of NO in the regulation of nitrosocysteine and BK channel protein in the magnocellular system in dehydrated animals. Using Western blot analysis and quantitative immunofluorescent staining study, we found that water deprivation in rats significantly enhanced the expression of nitrosocysteine protein in SON and neural lobes. Immunohistochemistry study indicated that dehydration significantly increased the profiles of SON neurons co-expressing nitrosocysteine with BK-channel protein. Intracerebroventricular administration of L-NAME (an inhibitor of NO synthase) significantly reduced the neuronal profiles of nitrosocysteine, as well as their co-expression with BK-channel in SON of dehydrated rats. However, treatment of sodium nitroprusside (a donor of NO) increased this co-expression. Our results indicate that NO signaling cascade may control the expression of BK channels through the regulation of nitrosocysteine in SON and neural lobe of rats during osmotic regulation.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-10517809, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-10651830, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-10718923, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-10835040, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-11086993, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-11175752, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-11562475, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-11572774, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-12498886, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-12727142, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-14766175, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-14769377, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-15064807, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-15699347, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-1718335, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-3815081, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-7509733, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-7511350, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-7526751, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-7584911, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-7732599, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-8545081, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-8789272, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-8807400, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-9182795, http://linkedlifedata.com/resource/pubmed/commentcorrection/17098363-9222524
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
411
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
117-22
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:17098363-Analysis of Variance, pubmed-meshheading:17098363-Animals, pubmed-meshheading:17098363-Blotting, Western, pubmed-meshheading:17098363-Cell Count, pubmed-meshheading:17098363-Cysteine, pubmed-meshheading:17098363-Dehydration, pubmed-meshheading:17098363-Enzyme Inhibitors, pubmed-meshheading:17098363-Fluorescent Antibody Technique, pubmed-meshheading:17098363-Gene Expression, pubmed-meshheading:17098363-Male, pubmed-meshheading:17098363-NG-Nitroarginine Methyl Ester, pubmed-meshheading:17098363-Nitric Oxide, pubmed-meshheading:17098363-Nitric Oxide Donors, pubmed-meshheading:17098363-Nitroprusside, pubmed-meshheading:17098363-Pituitary Gland, Posterior, pubmed-meshheading:17098363-Potassium Channels, Calcium-Activated, pubmed-meshheading:17098363-Rats, pubmed-meshheading:17098363-Rats, Sprague-Dawley, pubmed-meshheading:17098363-S-Nitrosothiols, pubmed-meshheading:17098363-Supraoptic Nucleus
pubmed:year
2007
pubmed:articleTitle
Effects of nitric oxide on expressions of nitrosocysteine and calcium-activated potassium channels in the supraoptic nuclei and neural lobe of dehydrated rats.
pubmed:affiliation
Division of Neurosurgery, Department of Surgery, The University of Texas Medical Branch, Galveston, TX 77555, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural