Licking for taste solutions by potassium-deprived rats: specificity and mechanisms.

There has been little work on the specificity and mechanisms underlying the appetite of potassium (K(+)) deprived rats, and there are conflicting results. To investigate the contribution of oral factors to changes in intake induced by K(+) deficiency, we conducted two experiments using 20-s "brief access" tests. In Experiment 1, K(+)-deprived rats licked less for water than did replete rats. After adjusting for this difference, K(+)-deprived rats exhibited increased licking for 100 mM CaCl(2), 100 mM MgCl(2), and 100 mM FeCl(2) compared with K(+)-replete rats. In Experiment 2, which used larger rats, the K(+)-deprived and replete groups licked equally for water, 500 mM Na.Gluconate, 350 mM KCl, 500 mM KHCO(3), and 1 mM quinine.HCl, but the K(+)-deprived rats licked more for 500 mM KCl, 500 mM CsCl, and 500 mM NaCl than did the replete rats. Licking was unaffected by addition to NaCl of 200 muM amiloride, an epithelial Na(+) channel (ENaC) blocker, or 100 muM ruthenium red, a vanilloid receptor 1 (VR-1) antagonist, or by addition to KCl of 50 muM 4-aminopyridine, a K(+) channel blocker. These findings suggest that K(+)-deprivation produces a non-specific appetite that is guided by oral factors. We found no evidence that this response was mediated by ENaC, VR-1, or K(+) channels in taste receptor cells.