and PtdInsP remained constant. Our results show that PtdInsP 2 is not volume sensitive per se, and moreover that the regulatory volume adjustments in Ehrlich ascites cells are not mediated by PtdInsP 2 hydrolysis and its subsequent production of second messengers. The simplest interpretation of the observed effects would be that PtdInsP 2 is controlled by ionic strength, probably via activation/inhibition of phosphoinositide-specific phosphatases/kinases. In Ehrlich ascites cells, as shown previously, the opposing ion channels and transporters activated during RVD and RVI, respectively, are controlled with tight negative coordination by a common cell volume 'set-point' that is shifted in anisotonic media, but unchanged during cell swelling in isosmotic high K + medium. We hypothesize that PtdInsP 2 might orchestrate this 'set-point' shift.