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 Ca2+ 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 NO3−. Removal of external Ca2+ during treatment with ATP reduced the fractional efflux of K+(Rb+) in a manner suggesting a role for cellular Ca2+ 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.