| pubmed-article:17023511 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17023511 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:17023511 | lifeskim:mentions | umls-concept:C0042401 | lld:lifeskim |
| pubmed-article:17023511 | lifeskim:mentions | umls-concept:C0221912 | lld:lifeskim |
| pubmed-article:17023511 | lifeskim:mentions | umls-concept:C0164209 | lld:lifeskim |
| pubmed-article:17023511 | lifeskim:mentions | umls-concept:C0205177 | lld:lifeskim |
| pubmed-article:17023511 | lifeskim:mentions | umls-concept:C1709852 | lld:lifeskim |
| pubmed-article:17023511 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:17023511 | pubmed:issue | Pt 3 | lld:pubmed |
| pubmed-article:17023511 | pubmed:dateCreated | 2006-12-15 | lld:pubmed |
| pubmed-article:17023511 | pubmed:abstractText | To date, the neurotransmitter(s) and pathways involved in cutaneous active vasodilatation are not fully understood. The purpose of this study was to determine the potential involvement of neurokinin-1 (NK(1)) receptors to active vasodilatation. Our experimental model exploited our previous findings that repeated microdialysis infusions of substance P desensitize the NK(1) receptors and that substance P-induced vasodilatation contains a substantial nitric oxide (NO) component. Eleven subjects were equipped with four microdialysis fibres on the ventral forearm. Site 1 served as a control and received a continuous infusion of Ringer solution. Site 2 received a continuous infusion of 10 mM L-NAME to inhibit NO synthase. Site 3 received a 10 microm dose of substance P to desensitize the NK(1) receptors prior to whole-body heating. Site 4 received a 10 microm dose of substance P combined with 10 mM L-NAME. Red blood cell (RBC) flux was measured via laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as RBC flux/mean arterial pressure and normalized to maximal vasodilatation via 28 mM sodium nitroprusside. Substance P was infused for 15 min at 4 microl min(-1) in sites 3 and 4, and skin blood flow was allowed to return to baseline (approximately 45-60 min). Subjects then underwent a period of whole-body heat stress to raise oral temperature 0.8-1.0 degrees C above baseline. Pretreatment with substance P increased CVC to 48 +/- 2% CVC(max), which was significantly greater than for sites pretreated with substance P combined with L-NAME (27 +/- 2% CVC(max); P < 0.001). During whole-body heating, CVC in control sites increased to 69 +/- 3% CVC(max). Sites pretreated with substance P (48 +/- 3% CVC(max)) were significantly reduced compared to control sites (P < 0.001). The CVC response to whole-body heat stress in L-NAME sites was significantly reduced (32 +/- 3% CVC(max); P < 0.001) compared to both control sites and sites pretreated with substance P. The CVC response to whole-body heating was nearly abolished in sites pretreated with substance P combined with L-NAME (20 +/- 2% CVC(max)) and was significantly reduced compared to the other three sites (all P < 0.001). These data suggest NK(1) receptors contribute to active vasodilatation and that combined NK(1) receptor desensitization and NO synthase inhibition further diminishes active vasodilatation. | lld:pubmed |
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| pubmed-article:17023511 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17023511 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17023511 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17023511 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17023511 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17023511 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:17023511 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:17023511 | pubmed:author | pubmed-author:MinsonChristo... | lld:pubmed |
| pubmed-article:17023511 | pubmed:author | pubmed-author:WongBrett JBJ | lld:pubmed |
| pubmed-article:17023511 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17023511 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:17023511 | pubmed:volume | 577 | lld:pubmed |
| pubmed-article:17023511 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17023511 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17023511 | pubmed:pagination | 1043-51 | lld:pubmed |
| pubmed-article:17023511 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17023511 | pubmed:meshHeading | pubmed-meshheading:17023511... | lld:pubmed |
| pubmed-article:17023511 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:17023511 | pubmed:articleTitle | Neurokinin-1 receptor desensitization attenuates cutaneous active vasodilatation in humans. | lld:pubmed |
| pubmed-article:17023511 | pubmed:affiliation | Department of Human Physiology, 122 C Esslinger Hall, 1240 University of Oregon, Eugene, OR 97403, USA. | lld:pubmed |
| pubmed-article:17023511 | pubmed:publicationType | Journal Article | lld:pubmed |
