Exogenous nitric oxide inhibits sympathetically mediated vasoconstriction in human skin.

Two experiments were performed to identify whether nitric oxide (NO) inhibits sympathetically mediated vasoconstriction in human skin. In eight subjects increasing doses of sodium nitroprusside (SNP; 8.4 x 10(-6)-8.4 x 10(-3)m) 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 8.4 x 10(-4)m (control: 63.0 +/- 4.1%, SNP 8.4 x 10(-6)m: 57.1 +/- 4.7%, SNP 8.4 x 10(-5)m: 57.0 +/- 3.6%, SNP 8.4 x 10(-4)m: 44.5 +/- 5.4% and SNP 8.4 x 10(-3)m: 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 seven 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(-1) (AU, arbitrary units), P > 0.05) or following drug infusion (SNP: 1.36 +/- 0.21; ISO: 1.27 +/- 0.23 AU mmHg(-1), 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.