Linked Life Data

16938283

Source:http://linkedlifedata.com/resource/pubmed/id/16938283

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-10-2
pubmed:abstractText
Upon return from spaceflight or resumption of normal posture after bed rest, individuals often exhibit cardiovascular deconditioning. Although the mechanisms responsible for cardiovascular deconditioning have yet to be fully elucidated, alterations within the central nervous system have been postulated to be involved. The paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus are important brain regions in control of sympathetic outflow and body fluid homeostasis. Nitric oxide (NO) modulates the activity of PVN and SON neurons, and alterations in NO transmission within these brain regions may contribute to symptoms of cardiovascular deconditioning. The purpose of the present study was to examine nitric oxide synthase (NOS) activity and expression in the PVN and SON of control and hindlimb unloaded (HU) rats, an animal model of cardiovascular deconditioning. The number of neurons exhibiting NOS activity as assessed by NADPH-diaphorase staining was significantly greater in the PVN but not SON of HU rats. Western blot analysis revealed that neuronal NOS (nNOS) but not endothelial NOS (eNOS) protein expression was higher in the PVN of HU rats. In the SON, there was a strong trend for an increase in nNOS (p=0.052) and a significant increase in eNOS expression in HU rats. Our results suggest that increased nNOS in the PVN contributes to autonomic and humoral alterations following cardiovascular deconditioning. In contrast, the functional significance of increases in nNOS and eNOS protein in the SON may be related to alterations in vasopressin release observed previously in HU rats.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
1115
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
65-74
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16938283-Animals, pubmed-meshheading:16938283-Cardiovascular Deconditioning, pubmed-meshheading:16938283-Cardiovascular Physiological Phenomena, pubmed-meshheading:16938283-Disease Models, Animal, pubmed-meshheading:16938283-Hindlimb Suspension, pubmed-meshheading:16938283-Immunohistochemistry, pubmed-meshheading:16938283-Male, pubmed-meshheading:16938283-NADPH Dehydrogenase, pubmed-meshheading:16938283-Neurons, pubmed-meshheading:16938283-Nitric Oxide, pubmed-meshheading:16938283-Nitric Oxide Synthase, pubmed-meshheading:16938283-Nitric Oxide Synthase Type I, pubmed-meshheading:16938283-Nitric Oxide Synthase Type III, pubmed-meshheading:16938283-Paraventricular Hypothalamic Nucleus, pubmed-meshheading:16938283-Rats, pubmed-meshheading:16938283-Rats, Sprague-Dawley, pubmed-meshheading:16938283-Supraoptic Nucleus, pubmed-meshheading:16938283-Sympathetic Nervous System, pubmed-meshheading:16938283-Up-Regulation, pubmed-meshheading:16938283-Water-Electrolyte Balance, pubmed-meshheading:16938283-Weight-Bearing, pubmed-meshheading:16938283-Weightlessness, pubmed-meshheading:16938283-Weightlessness Simulation
pubmed:year
2006
pubmed:articleTitle
Increased nitric oxide synthase activity and expression in the hypothalamus of hindlimb unloaded rats.
pubmed:affiliation
Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211-3300, USA. MuellerP@missouri.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural