Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

D. L. Kellogg, Y. Liu, K. McAllister, C. Friel, P. E. Pérgola

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 μM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P < 0.01) and untreated sites (65 ± 2% maximal CVC, P < 0.01). These responses did not differ between sites (P > 0.05). Because the bradykinin B2-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.

Original languageEnglish (US)
Pages (from-to)1215-1221
Number of pages7
JournalJournal of applied physiology
Issue number4
StatePublished - Oct 2002


  • Laser-Doppler flowmetry
  • Microdialysis

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


Dive into the research topics of 'Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans'. Together they form a unique fingerprint.

Cite this