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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-6-17
pubmed:abstractText
Vascular endothelial growth factor (VEGF) is considered to be important in promotion of capillary growth in skeletal muscles exposed to increased activity. We studied its interactions with nitric oxide (NO) by examining the expression of endothelial NO synthase (NOS), VEGF, and VEGF receptor-2 (VEGFR-2) proteins in relation to capillary growth in rat extensor digitorum longus muscles electrically stimulated for 2, 4, or 7 days with and without NOS inhibition by N(omega)-nitro-L-arginine (L-NNA, 3 mg/day). Stimulation increased all proteins from 2 days onward, concomitantly with capillary proliferation (labeling for proliferating cell nuclear antigen). Capillary-to-fiber ratio was elevated by 25% after 7 days. Concurrent oral administration of L-NNA did not affect the increase in endothelial NOS but depressed its activity, as shown by increased blood pressure and decreased arteriolar diameters in 2-day-stimulated muscles. NOS inhibition eliminated the increased expression of VEGFR-2 and VEGF proteins in muscles stimulated for 2 and 4 days but not for 7 days. However, it depressed capillary proliferation and the increase in C/F at all time points. We conclude that, in stimulated muscles, NO, generated by activation of neuronal NOS by muscle activity or endothelial NOS by increased blood flow and capillary shear stress, may increase capillary proliferation in the early stages of stimulation through upregulation of VEGFR-2 and VEGF. With longer stimulation, capillary growth appears to require NO, and high levels of VEGF and VEGFR-2 may be contributing to maintenance of the increased capillary bed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
289
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H336-43
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15734877-Animals, pubmed-meshheading:15734877-Arterioles, pubmed-meshheading:15734877-Blood Pressure, pubmed-meshheading:15734877-Blotting, Western, pubmed-meshheading:15734877-Capillaries, pubmed-meshheading:15734877-Cell Division, pubmed-meshheading:15734877-Drug Interactions, pubmed-meshheading:15734877-Enzyme Inhibitors, pubmed-meshheading:15734877-Male, pubmed-meshheading:15734877-Muscle, Skeletal, pubmed-meshheading:15734877-Neovascularization, Physiologic, pubmed-meshheading:15734877-Nitric Oxide, pubmed-meshheading:15734877-Nitroarginine, pubmed-meshheading:15734877-Rats, pubmed-meshheading:15734877-Rats, Sprague-Dawley, pubmed-meshheading:15734877-Vascular Endothelial Growth Factor A, pubmed-meshheading:15734877-Vascular Endothelial Growth Factor Receptor-2, pubmed-meshheading:15734877-Vasodilation
pubmed:year
2005
pubmed:articleTitle
Nitric oxide, VEGF, and VEGFR-2: interactions in activity-induced angiogenesis in rat skeletal muscle.
pubmed:affiliation
Dept. of Physiology, Univ. of Birmingham Medical School, Birmingham B15 2TT, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't