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 pH_i may be decisive in the transduction of nociception and pain from tissue acidosis.