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Received September 17, 2004
Revised October 7, 2004
Accepted after revision November 8, 2004
1 Presbyterian Hospital of Dallas
* To whom correspondence should be addressed. E-mail: craigcrandall{at}texashealth.org.
Two experiments were performed to identify whether nitric oxide (NO) inhibits sympathetically-mediated vasoconstriction in human skin. In 8 subjects increasing doses of sodium nitroprusside (SNP; 8.4x10-6 to 8.4x10-3M) were administered via intradermal microdialysis. At each dose of SNP, cutaneous vasoconstrictor responsiveness was assessed during a 3-min whole-body cold stress. The relative reduction in forearm cutaneous vascular conductance (CVC) during the cold stress was significantly attenuated for SNP doses greater than 8.4x10-4M (Control: 63.0±4.1%, SNP 8.4x10-6M: 57.1±4.7%, SNP 8.4x10-5M: 57.0±3.6%, SNP 8.4x10-4M: 44.5±5.4% and SNP 8.4x10-3M: 28.8±7.9%). The second experiment was performed to identify whether this response was due to NO attenuating sympathetically mediated vasoconstriction or due to a non-specific effect of an elevated CVC secondary to SNP administration. In 7 subjects forearm CVC during a whole-body cold stress was assessed at two sites; at a site dilated via microdialysis administration of SNP and at a site dilated with isoproterenol (ISO). CVC was not different between sites prior to (SNP: 0.42±0.11; ISO: 0.46±0.11 AU/mmHg, P> 0.05) or following drug infusion (SNP: 1.36±0.21; ISO: 1.27±0.23 AU/mmHg, P> 0.05). The reduction in CVC during the subsequent cold stress was significantly less at the SNP site (38.1±6.2%) relative to the ISO site (65.0±5.5%; P=0.007). These data suggest NO is capable of inhibiting sympathetically-mediated vasoconstriction in the cutaneous vasculature.
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