Influence of calcium on regulatory volume decrease: role of potassium channels.

Abstract

In most cell types, hyposmotic swelling consistently elicits an increase in the concentration of cytosolic Ca2+ - [Ca2+]i - with contributions of extracellular and intracellular sources. The mechanisms of Ca2+ entry and release from endogenous sources are not fully clarified and may be cell specific. The ubiquity of the swelling-evoked [Ca2+]i rise makes Ca2+ a likely candidate for a role as osmotransducing signal. However, the regulatory volume decrease (RVD) which follows swelling and the osmolyte fluxes involved in this process are not always Ca2+ dependent. It was found that, with a few exceptions, in most cell types the osmosensitive Cl- efflux pathway and the swelling-activated organic osmolyte fluxes are Ca2+ independent. In contrast, Ca2+-dependent or Ca2+-independent K+ fluxes activated by swelling are detected, depending on the cell type. The close correlation found in this review between the Ca2+ dependence of RVD and that of the K+ channels activated by swelling led to the conclusion that it is the type of osmosensitive K+ pathway which largely confers the Ca2+ dependence to RVD. Interestingly, this coincidence of Ca2+-dependent K+ efflux and RVD is found predominantly in epithelial cells, whereas in nonepithelial cells both processes are largely Ca2+ independent. In these cells, the [Ca2+]i rise elicited by swelling may be an epiphenomenon.