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The pH response of rat cutaneous nociceptors correlates with extracellular [Na+] and is increased under amiloride

Authors

  • Kay H. Steen,

    1. Klinik und Poliklinik für Dermatologie der Universität Bonn, Klinische Dermatophysiologie, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany
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  • Holger Wegner,

    1. Klinik und Poliklinik für Dermatologie der Universität Bonn, Klinische Dermatophysiologie, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany
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  • Peter W. Reeh

    1. Institut für Physiologie & Experimentelle Pathophysiologie der Universität Erlangen-Nürnberg, Universitätsstrasse 17, D-91054 Erlangen, Germany
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: Dr Kay H. Steen, as above.
E-mail: khsteen@mailer.meb.uni-bonn.de

Abstract

Excess hydrogen ions induce sustained nociceptor excitation as well as pain, and this has been suggested, with evidence from sensory ganglion cells, to result from gating a slowly inactivating sodium/calcium inward current. In the rat skin-nerve preparation, isolated receptive fields of pH-sensitive C-fibre terminals were exposed to low-pH solutions of various sodium concentrations. The pH responses showed a good correlation with log [Na+]e, which supports the above model. Amiloride has previously been shown to block a pH-induced Na+ current involved in sensory transduction in hamster taste cells; however, it has been shown to act differently in cutaneous nociceptors. Amiloride induced a dose-dependent increase in and prolongation of the nociceptive pH responses, with a prominent acceleration of the onset. The latter could be mimicked by replacing external sodium with sucrose, thus impeding sodium-proton antiport. Together, the findings indicate functional expression of amiloride-sensitive Na+/H+-antiporters, which enable the nociceptive nerve endings to extrude invading H+. Intracellular acidification may thus compete with Na+/H+ exchange, and pHi may be decisive in the transduction of nociception and pain from tissue acidosis.

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