K-induced alkalinization in all cell types of rabbit gastric glands: A novel K/H exchange mechanism.

Digital image processing of the pH-sensitive dye BCECF was used to examine the effects of high [K] media on cytoplasmic pH (pH) of individual cells within isolated rabbit gastric glands. When cells were acidified to pH 6.5 from the resting pH of 7.2-7.3 and then exposed to solution containing 77 m m K plus amiloride (to block Na/H exchange), recovery to pH 7.0 was observed. This K-induced alkalinization occurred in all cell types of the gland, including cells within antral glands that were devoid of parietal cells (PC). This process was independent of extracellular Na and Cl and was unaffected by: 5 m m Ba or 200 μ m bumetanide, or acute treatment with either 500 μ m ouabain or 100 μ m cimetidine, histamine or carbachol. SCH28080, which inhibits the PC H/K-ATPase when used in the low μ m range of concentrations, blocked the K effect on pH, at 100 μ m but was ineffective at 1 μ m. A similar pH recovery was also stimulated by Li, Cs (both 72 m m), and Tl (10 m m), in the order Li>K> Cs>Tl (all in the presence of amiloride), and these alkalinizations were also blocked by 100 μ m SCH28080. Parallel experiments were performed to test the effect of these ions on [C]-aminopyrine accumulation, an index of acid secretion by the H/K-ATPase at the lumenal membrane of the PC. There was no correlation between the rates of cation-induced pH recovery from an acid load and H secretion as measured by the accumulation of aminopyrine. We conclude that the K (and Cs-and Li-) dependent pH recovery is mediated by a novel cation/H exchange mechanism that is distinct from the PC H/K-ATPase. [ABSTRACT FROM AUTHOR]