Exogenous nitric oxide inhibits sympathetically mediated vasoconstriction in human skin

S. Durand, S. L. Davis, J. Cui, C. G. Crandall

Research output: Contribution to journalArticle

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Abstract

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 × 10-6-8.4 × 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 × 10-4 M (control: 63.0 ± 4.1%, SNP 8.4 × 10-6 M: 57.1 ± 4.7%, SNP 8.4 × 10-5 M: 57.0 ± 3.6%, SNP 8.4 × 10-4 M: 44.5 ± 5.4% and SNP 8.4 × 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.

Original languageEnglish (US)
Pages (from-to)629-634
Number of pages6
JournalJournal of Physiology
Volume562
Issue number2
DOIs
StatePublished - Jan 15 2005

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Vasoconstriction
Single Nucleotide Polymorphism
Nitric Oxide
Skin
Blood Vessels
Isoproterenol
Microdialysis
Forearm
Nitroprusside
Vasoconstrictor Agents

ASJC Scopus subject areas

  • Physiology

Cite this

Exogenous nitric oxide inhibits sympathetically mediated vasoconstriction in human skin. / Durand, S.; Davis, S. L.; Cui, J.; Crandall, C. G.

In: Journal of Physiology, Vol. 562, No. 2, 15.01.2005, p. 629-634.

Research output: Contribution to journalArticle

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abstract = "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 × 10-6-8.4 × 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 × 10-4 M (control: 63.0 ± 4.1{\%}, SNP 8.4 × 10-6 M: 57.1 ± 4.7{\%}, SNP 8.4 × 10-5 M: 57.0 ± 3.6{\%}, SNP 8.4 × 10-4 M: 44.5 ± 5.4{\%} and SNP 8.4 × 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.",
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