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

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 > or = 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 x 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.