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.

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