Effect of amiloride on the taste of NaCl, Na-gluconate and KCl in humans: implications for Na+ receptor mechanisms.

Abstract

Sodium-salt transduction in many species may be mediated by both apical and submucosal ion channels on the taste receptor cell membrane. The apical ion channel is blockable by the diuretic amiloride, whereas the submucosal pathway is not. Sodium salts with small anions, such as NaCl, can stimulate submucosal as well as apical ion channels; sodium salts with large anions, such as Na-gluconate, activate primarily the apical channels. In humans, reports on the effects of amiloride on the taste of NaCl are conflicting and no data exist on the effects of amiloride on organic sodium salts. In the present experiment, subjects gave magnitude estimates of the total intensity and of each of the basic taste qualities for NaCl, Na-gluconate and KCl. Five concentrations of each of these stimuli were presented to the anterior tongue following distilled water adaptation and after amiloride treatment. There was a significant decrease in the total taste intensity of NaCl and Na-gluconate after amiloride, but no effect on KCl. The saltiness of all three salts was unaffected, but amiloride decreased the perceived sourness of the sodium salts. KCl sourness was unaffected by amiloride. There was a proportionately larger effect of amiloride on Na-gluconate than on NaCl, which is consistent with a larger role for the apical ion channel in Na-gluconate transduction. However, an appreciable amiloride-insensitive component is present for both NaCl and Na-gluconate, suggesting that an amiloride-insensitive pathway also plays a role in the transduction of both sodium salts. These data support the hypothesis that an amiloride-sensitive transduction component exists in humans, but suggest that it is considerably smaller than in many other species.