Separate, Ca2+-activated K+ and Cl− transport pathways in Ehrlich ascites tumor cells | Semantic Scholar (2024)

The results indicate that the stimulation of the Na+, K+, Cl− cotransport involves both Ca2+/calmodulin and protein kinase C.

It is shown that CuSO4 inhibits RVD as a result of a net uptake of sodium, of which the major part is sensitive to amiloride, and it is concluded that this mechanism is a Na+/H+ exchange system, activated by cytoplasmic acidification.

Although ouabain has no effect on volume recovery, bumetanide completely blocks RVI by inhibiting a cotransport pathway that mediates the net uptake of Na+, K+ and Cl− in the ratio of 1Na∶1K∶2Cl.

Cell-attached patch-clamp recordings from Ehrlich ascites tumor cells reveal nonselective cation channels which are activated by mechanical deformation of the membrane, and singlechannel currents with characteristics similar to the channels seen in isolated patches are seen.

The taurine efflux from Ehrlich ascites tumor cells is stimulated by hypotonic cell swelling and a swelling-activated “Mini Cl− channel” is suggested, which is suggested to represent two distinct types of channels.

It is shown that cell volume regulation is controlled by processes involving Cl− and K+ excretion through conductive pathways, and that cells completely maintained their ability to regulate their volume after replacing Cl− by NO3−.

The cell membrane is depolarized by addition of the K+ channel inhibitor quinine and it is hyperpolarized when the cells are suspended in Na+-free choline medium, indicating that Vm is generated partly by potassium and partly by sodium diffusion.

It is suggested that in ELA cells, entrance into the S phase requires an increase in VRAC activity and/or an increased potential for regulatory volume decrease (RVD), and at the same time a decrease in CaCC magnitude.

It is concluded that the swelling-induced activation of the taurine leak pathway involves a release of arachidonic acid from the membrane phospholipids and an increased oxidation of aracheric acid into leukotrienes via the 5-lipoxygenase pathway.

It is proposed that inhibition of RVD in hypotonic media by arachidonic acid is caused by reduction in the volume-induced Cl and K permeabilities as well as by an increase in Na permeability and that reduction in A23187 + Ca-induced cell shrinkage is due to a reduction in K permeability

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It is proposed that separate conductive K+ and Cl− channels are activated during regulatory volume decrease by release of Ca2+ from internal stores, and that the effect is mediated by calmodulin.

It is proposed that the primary process during the regulatory volume increase is an activation of an otherwise quiescent, bumetanide-sensitive Na+, Cl− cotransport system with subsequent replacement of Na+ by K+ via the Na+/K+ pump, stimulated by the Na+.

The combined results show that Ehrlich cells possess a latent K-Cl cotransport that becomes active after changes in the state of SH groups, regardless of the initial cell volume, and seems to inhibit a Cl-dependent Na uptake previously described in shrunken cells.

The inhibitory activity of the latter drugs, which are powerful antagonists of calmodulin, suggests the participation of this Ca2+-regulator protein in volume regulation.

The regulatory volume decrease of osmotically swollen human peripheral blood lymphocytes can be inhibited by agents acting on volume-activated K+- or Cl--transport pathways, and the inhibition characteristics of the volume-induced K+ pathway of lymphocytes resemble those of the Ca2+- activated K+ channel of red cells.

It is concluded that at least two distinct Cl- -dependent transport pathways for K+ are inducible in mammalian red cells, although the evidence for their separation is not absolute.

Kinetic studies of swollen cells indicate that N E addition causes the swelling-induced K transport to be replaced by [Na + K + 2Cl] cotransport, confirming the previous conclusion that [Na = 2Cl + 1C1 + 2C1] cOTransport is electrically neutral.

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