摘要

Intracellular pH (pH(i)) regulation fundamentally participates in maintaining HCO3 (-) release from HCO3 (-)-secreting epithelia. We used parotid intralobular ducts loaded with BCECF to investigate the contributions of a carbonic anhydrase (CA), anion channels and a Na+-H+ exchanger (NHE) to pH(i) regulation for HCO3 (-) secretion by cAMP and Ca2+ signals. Resting pH(i) was dispersed between 7.4 and 7.9. Forskolin consistently decreased pH(i) showing the dominance of pH(i)-lowering activities, but carbachol gathered pH(i) around 7.6. CA inhibition suppressed the forskolin-induced decrease in pH(i), while it allowed carbachol to consistently increase pH(i) by revealing that carbachol prominently activated NHE via Ca2+-calmodulin. Under NHE inhibition, forskolin and carbachol induced the remarkable decreases in pH(i), which were slowed predominantly by CA inhibition and by CA or anion channel inhibition, respectively. Our results suggest that forskolin and carbachol primarily activate the pH(i)-lowering CA and pH(i)-raising NHE, respectively, to regulate pH(i) for HCO3 (-) secretion.

  • 出版日期2016-11