Nitric oxide and cutaneous active vasodilation during heat stress in humans

D. L. Kellogg, C. G. Crandall, Y. Liu, N. Charkoudian, J. M. Johnson

Research output: Contribution to journalArticlepeer-review

259 Scopus citations


Whether nitric oxide (NO) is involved in cutaneous active vasodilation during hyperthermia in humans is unclear. We tested for a role of NO in this process during heat stress (water-perfused suits) in seven healthy subjects. Two forearm sites were instrumented with intradermal microdialysis probes. One site was perfused with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) dissolved in Ringer solution to abolish NO production. The other site was perfused with Ringer solution only. At those sites, skin blood flow (laser-Doppler flowmetry) and sweat rate were simultaneously and continuously monitored. Cutaneous vascular conductance, calculated from laserDoppler fiowmetry and mean arterial pressure, was normalized to maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions, L-NAME did not significantly reduce cutaneous vascular conductance. During hyperthermia, with skin temperature held at 38-38.5°C, internal temperature rose from 36.66 ± 0.10 to 37.34 ± 0.06°C (P < 0.01). Cutaneous vascular conductance at untreated sites increased from 12 ± 2 to 44 ± 5% of maximum, but only rose from 13 ± 2 to 30 ± 5% of maximum at L-NAME-treated sites (P < 0.05 between sites) during heat stress. L-NAME had no effect on sweat rate (P > 0.05). Thus cutaneous active vasodilation requires functional NO synthase to achieve full expression.

Original languageEnglish (US)
Pages (from-to)824-829
Number of pages6
JournalJournal of applied physiology
Issue number3
StatePublished - Sep 1998


  • Laser-Doppler flowmetry
  • Microdialysis
  • Skin blood flow

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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