抄録
In many epithelial cells, intracellular Cl− concentration ([Cl−]i) is maintained by Na+/K+/2Cl− cotransport (NKCC, influx) and Cl− channels (efflux). Inhibition of NKCC (bumetanide) decreased [Cl−]i and inhibition of Cl− channels increased it. Our recent studies demonstrated that bumetanide (20 μM) or a Cl−-free (NO3−) solution enhanced ACh-stimulated exocytosis in guinea pig antral mucous cells, in contrast, NPPB (a Cl− channel blocker) decreased it and eliminated the enhancement induced by bumetanide or NO3− solution. An [Cl−]i decrease modulates ATP-dependent priming in Ca2+-regulated exocytosis. And, [Ca2+]i measurements showed that bumetanide and NO3− solution enhanced the ACh-stimulated [Ca2+]i increase. Measurements of [Cl−]i revealed that ACh decreases [Cl−]i, and that bumetanide and NO3− solution decreased [Cl−]i and enhanced the ACh-evoked [Cl−]i decrease; in contrast, NPPB increased [Cl−]i and inhibited the [Cl−]i decrease induced by ACh, bumetanide or NO3− solution. Thus, an [Cl−]i decrease accelerates ATP-dependent priming and [Ca2+]i increase, which enhance Ca2+-regulated exocytosis in ACh-stimulated antral mucous cells. Moreover, in bronchiolar ciliary cells, an [Cl−]i decrease also enhanced ciliary beat frequency by modulating cAMP actions. These observations indicate that the Cl− transport plays an important role in the regulation of cellular functions in epithelia. [J Physiol Sci. 2008;58 Suppl:S22]
