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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 3
pubmed:dateCreated
2006-12-15
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.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-10194201, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-10336084, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-10658012, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-11121135, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-11568143, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12381749, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12391110, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12651918, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12679350, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12692141, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12808346, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12847205, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-12849662, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-13414140, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-13429515, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-13564431, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-14715681, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-15155712, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-15375193, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-16109832, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-16123103, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-16484440, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-1692268, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-1702831, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-1706332, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-17095556, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-1711051, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-1718893, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-2428650, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-2442929, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-3153452, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-6104898, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-6154244, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-7523474, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-7534932, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-7542531, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-7586235, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-8800300, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-9312403, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-9457475, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-9574822, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-9729553, http://linkedlifedata.com/resource/pubmed/commentcorrection/17023511-9729554
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
577
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1043-51
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:17023511-Adult, pubmed-meshheading:17023511-Blood Pressure, pubmed-meshheading:17023511-Enzyme Inhibitors, pubmed-meshheading:17023511-Erythrocytes, pubmed-meshheading:17023511-Female, pubmed-meshheading:17023511-Hot Temperature, pubmed-meshheading:17023511-Humans, pubmed-meshheading:17023511-Laser-Doppler Flowmetry, pubmed-meshheading:17023511-Male, pubmed-meshheading:17023511-NG-Nitroarginine Methyl Ester, pubmed-meshheading:17023511-Nitric Oxide Donors, pubmed-meshheading:17023511-Nitric Oxide Synthase, pubmed-meshheading:17023511-Nitroprusside, pubmed-meshheading:17023511-Receptors, Neurokinin-1, pubmed-meshheading:17023511-Regional Blood Flow, pubmed-meshheading:17023511-Skin, pubmed-meshheading:17023511-Stress, Physiological, pubmed-meshheading:17023511-Substance P, pubmed-meshheading:17023511-Vasodilation
pubmed:year
2006
pubmed:articleTitle
Neurokinin-1 receptor desensitization attenuates cutaneous active vasodilatation in humans.
pubmed:affiliation
Department of Human Physiology, 122 C Esslinger Hall, 1240 University of Oregon, Eugene, OR 97403, USA.
pubmed:publicationType
Journal Article
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