The effect of a hyposmotic shock and purinergic agonists on K+(Rb+) efflux from cultured human breast cancer cells.

The effect of a hyposmotic shock and extracellular ATP on the efflux of K(+)(Rb(+)) from human breast cancer cell lines (MDA-MB-231 and MCF-7) has been examined. A hyposmotic shock increased the fractional efflux of K(+)(Rb(+)) from MDA-MB-231 cells via a pathway which was unaffected by Cl(-) replacement. Apamin, charybdotoxin or removing extracellular Ca(2+) had no effect on volume-activated K(+)(Rb(+)) efflux MDA-MB-231 cells. An osmotic shock also stimulated K(+)(Rb(+)) efflux from MCF-7 cells but to a much lesser extent than found with MDA-MB-231 cells. ATP-stimulated K(+)(Rb(+)) efflux from MDA-MB-231 cells in a dose-dependent fashion but had little effect on K(+)(Rb(+)) release from MCF-7 cells. ATP-stimulated K(+)(Rb(+)) efflux was only inhibited slightly by replacing Cl(-) with NO(3)(-). Removal of external Ca(2+) during treatment with ATP reduced the fractional efflux of K(+)(Rb(+)) in a manner suggesting a role for cellular Ca(2+) stores. Charybdotoxin, but neither apamin nor iberiotoxin, inhibited ATP-stimulated K(+)(Rb(+)) release from MDA-MB-231 cells. Suramin inhibited the ATP-activated efflux of K(+)(Rb(+)). UTP also stimulated K(+)(Rb(+)) efflux from MDA-MB-231 cells whereas ADP, AMP and adenosine were without effect. A combination of an osmotic shock and ATP increased the fractional efflux of K(+)(Rb(+)) to a level greater than the sum of the individual treatments. It appears that the hyposmotically-activated and ATP-stimulated K(+) efflux pathways are separate entities. However, there may be a degree of 'crosstalk' between the two pathways.