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This Article Full Text Full Text (PDF) All Versions of this Article: 575/3/953    most recent jphysiol.2006.112649v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shibasaki, M. Articles by Crandall, C. G. Search for Related Content PubMed PubMed Citation Articles by Shibasaki, M. Articles by Crandall, C. G. Related Collections Integrative

¹ Department of Environmental Health, Nara Women's University
² Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas
³ Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, TX, USA

Given the large increase in cutaneous vascular conductance (CVC) during whole-body heat stress, this vascular bed is important in the regulation of blood pressure during orthostatic stress. In this thermal state, changes in CVC are reported to be due to withdrawal of active vasodilator activity. The purpose of this study was to identify, contrary to the current line of thinking, whether cutaneous vasoconstrictor neural activity is enhanced and capable of contributing to reductions in CVC during an orthostatic challenge of heat-stressed individuals. Healthy normotensive subjects were pretreated, subcutaneously, with botulinum toxin A (BTX-A) to inhibit the release of neurotransmitters from cutaneous active vasodilator nerves. On the experimental day, microdialysis probes were placed in the BTX-A-treated site and in an adjacent untreated site. In protocol 1, internal temperature was elevated 0.7°C, followed by the application of lower body negative pressure (LBNP; –30 mmHg). LBNP reduced CVC at the BTX-A-treated sites (4.2 ± 2.9%max), as well as at the control site (9.8 ± 4.1%max). In protocol 2, after confirming the absence of cutaneous vasodilatation at the BTX-A-treated site during whole-body heating, CVC at this site was elevated to a similar level relative to the control site (55.4 ± 13.4 versus 60.7 ± 10.4%max, respectively) via intradermal administration of isoproterenol prior to LBNP. Similarly, when flow was matched between sites, LBNP reduced CVC at both the BTX-A-treated (15.3 ± 4.6%max) and the control sites (8.8 ± 5.6%max). These data suggest that the cutaneous vasoconstrictor system is engaged and is capable of decreasing CVC during an orthostatic challenge in heat-stressed individuals.

(Received 1 May 2006; accepted after revision 21 June 2006; first published online 22 June 2006)
Corresponding author C. G. Crandall: Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Ave., Dallas, TX 75231, USA. Email: craigcrandall{at}texashealth.org

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