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This Article Full Text Full Text (PDF) All Versions of this Article: 289/1/H174    most recent 01020.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Garry, A. Articles by Fromy, B. Search for Related Content PubMed PubMed Citation Articles by Garry, A. Articles by Fromy, B.

Cellular mechanisms underlying cutaneous pressure-induced vasodilation: in vivo involvement of potassium channels

Laboratory of Physiology, Unité Mixte de Recherche Centre National de la Recherche Scientifique 6188, School of Medicine, Angers, France

Submitted 6 October 2004 ; accepted in final form 18 February 2005

In the skin of humans and rodents, local pressure induces localized cutaneous vasodilation, which may be protective against pressure-induced microvascular dysfunction and lesion formation. Once activated by the local pressure application, capsaicin-sensitive nerve fibers release neuropeptides that act on the endothelium to synthesize and release nitric oxide (NO) and prostaglandins, leading to the development of the cutaneous pressure-induced vasodilation (PIV). The present study was undertaken to test in vivo the hypothesis that PIV is mediated or modulated by differential activation of K⁺ channels in anesthetized rats using pharmacological methods. Local pressure was applied at 11.1 Pa/s. Endothelium-independent and -dependent vasodilation were tested using iontophoretic delivery of sodium nitroprusside (SNP) and acetylcholine (ACh), respectively, and was correlated with PIV response. PIV was reduced after systemic administration of tetraethylammonium (a nonspecific K⁺ channel blocker), iberiotoxin [a specific large-conductance Ca²⁺-activated K⁺ (BK_Ca) channel blocker], and glibenclamide [a specific ATP-sensitive K⁺ (K_ATP) channel blocker], whereas PIV was unchanged by apamin (a specific small-conductance Ca²⁺-activated K⁺channel blocker) and 4-aminopyridine (a specific voltage-sensitive K⁺ channel blocker). The responses to SNP and ACh were reduced by iberiotoxin but were unchanged by glibenclamide. We conclude that the cellular mechanism of PIV in skin involves BK_Ca and K_ATP channels. We suggest that the opening of BK_Ca and K_ATP channels contributes to the hyperpolarization of vascular smooth muscle cells to produce PIV development mainly via the NO and prostaglandin pathways, respectively.

cutaneous blood flow; endothelium-dependent response; iontophoresis; microcirculation; rat