Journal of Applied Physiology
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J Appl Physiol 93: 1215-1221, 2002; doi:10.1152/japplphysiol.01142.2001
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Vol. 93, Issue 4, 1215-1221, October 2002

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

D. L. Kellogg Jr.1,2, Y. Liu2, K. McAllister2, C. Friel2, and P. E. Pérgola3

1 Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs, South Texas Veterans Health Care System, Audie L. Murphy Memorial Veterans Hospital Division, and Divisions of 2 Geriatrics and Gerontology and 3 Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229

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.

microdialysis; laser-Doppler flowmetry


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