Taste receptor cells (TRCs) respond to acid stimulation, initiating perception of sour taste. Paradoxically, the pH of weak acidic stimuli correlates poorly with the perception of their sourness. A fundamental issue surrounding sour taste reception is the identity of the sour stimulus. We tested the hypothesis that acids induce sour taste perception by penetrating plasma membranes as H(+) ions or as undissociated molecules and decreasing the intracellular pH (pH(i)) of TRCs. Our data suggest that taste nerve responses to weak acids (acetic acid and CO(2)) are independent of stimulus pH but strongly correlate with the intracellular acidification of polarized TRCs. Taste nerve responses to CO(2) were voltage sensitive and were blocked with MK-417, a specific blocker of carbonic anhydrase. Strong acids (HCl) decrease pH(i) in a subset of TRCs that contain a pathway for H(+) entry. Both the apical membrane and the paracellular shunt pathway restrict H(+) entry such that a large decrease in apical pH is translated into a relatively small change in TRC pH(i) within the physiological range. We conclude that a decrease in TRC pH(i) is the proximate stimulus in rat sour taste transduction.

. mRNA for two Na ϩ -H ϩ -exchanger isoforms 1 and 3 (NHE-1 and NHE-3) was detected by RT-PCR in fungiform and circumvallate taste receptor cells (TRCs). Anti-NHE-1 antibody binding was localized to the basolateral membranes, and the anti-NHE-3 antibody was localized in the apical membranes of fungiform and circumvallate TRCs. In a subset of TRCs, NHE-3 immunoreactivity was also detected in the intracellular compartment. For functional studies, an isolated lingual epithelium containing a single fungiform papilla was mounted with apical and basolateral sides isolated and perfused with nominally CO 2 /HCO 3 Ϫ -free physiological media (pH 7.4). The TRCs were monitored for changes in intracellular pH (pH i ) and Na The results indicate the presence of a functional NHE-1 in the basolateral membranes of TRCs. We hypothesize that NHE-1 is involved in sour taste transduction since its activity is modulated during acid stimulation.

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Male Sprague-Dawley rats (150-200 g) were randomly assigned to sham operation (n=6) or 5/6 nephrectomy (n=12) procedures. Two weeks after the completion of the 5/6 nephrectomy, these animals were again randomly assigned to two groups: non-treatment or treatment with vitamin E supplementation at 200 IU/kg chow. Two weeks later, all animals were sacrificed and the kidneys harvested. The secretory phospholipase A(2) (PLA(2)) activity was elevated (150%) in the untreated remnant kidney but returned to sham values in the vitamin E-treated kidneys. The cytoprotective heat shock protein (HSP70) and the intracellular antioxidant superoxide dismutase (MnSOD, Cu/ZnSOD) were similar in sham, remnant, and vitamin E-treated remnant kidneys. We conclude that the sudden reduction of renal mass secondary to the 5/6 nephrectomy procedure stimulates PLA(2) activity but not HSP70, MnSOD, or Cu/ZnSOD. This increased activity of PLA(2) in the remnant kidney returned to sham values after vitamin E treatment. The intrinsic cellular antioxidant enzymes, MnSOD, Cu/ZnSOD, as well as the cytoprotective heat shock protein HSP70, showed no significant changes in either vitamin E-treated or untreated kidneys compared with sham. These data are suggestive that the elevation of PLA(2) is a specific and localized response to the sudden reduction of renal mass.