Activation of water-responsive laryngeal afferents: role of epithelial ion transport

Abstract

The role of epithelial ion transport in the activation of water-responsive laryngeal afferent was investigated in anesthetized, spontaneously breathing cats. Single-fiber recordings from the peripheral cut-end of the superior laryngeal nerve were carried out to identify water-responsive laryngeal afferent. Substitution of chloride ions (Cl −) of the Krebs solution with gluconate activated the water-responsive endings when the gluconate concentration was ≥ 50 mM. Amiloride (10 −4, 10 −3 and 10 −2 M), an inhibitor of epithelial sodium channels, reduced the water-responsiveness of these afferents, whereas EIPA (5 × 10 −5 M), an amiloride analogue which inhibits Na +/H + exchange, had no effect. Both ouabain (10 −4 M), an inhibitor of Na +/K + ATPase, and bumetanide (10 −4 M), an inhibitor of Na +K +2Cl − cotransport, reduced the water response, but no significant reduction in the response was observed with DIDS and DPC, two chloride channel inhibitors. These findings suggest that the epithelium modulates the water-responsiveness of laryngeal afferent but is not the primary determinant of the response.