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Integrative |
1 Department of Human Physiology, University of Oregon, Eugene, OR, USA, 97403
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 (NK1) receptors to active vasodilatation. Our experimental model exploited our previous findings that repeated microdialysis infusions of substance P desensitize the NK1 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 µM dose of substance P to desensitize the NK1 receptors prior to whole-body heating. Site 4 received a 10 µM 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 µl min–1 in sites 3 and 4, and skin blood flow was allowed to return to baseline (
45–60 min). Subjects then underwent a period of whole-body heat stress to raise oral temperature 0.8–1.0°C above baseline. Pretreatment with substance P increased CVC to 48 ± 2% CVCmax, which was significantly greater than for sites pretreated with substance P combined with L-NAME (27 ± 2% CVCmax; P < 0.001). During whole-body heating, CVC in control sites increased to 69 ± 3% CVCmax. Sites pretreated with substance P (48 ± 3% CVCmax) 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% CVCmax; 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% CVCmax) and was significantly reduced compared to the other three sites (all P < 0.001). These data suggest NK1 receptors contribute to active vasodilatation and that combined NK1 receptor desensitization and NO synthase inhibition further diminishes active vasodilatation.
(Received 28 April 2006;
accepted after revision 29 September 2006;
first published online 5 October 2006)
Corresponding author C. T. Minson: Department of Human Physiology, 122 C Esslinger Hall, 1240 University of Oregon, Eugene, OR, USA. Email: minson{at}uoregon.edu
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