C. Hougaard et al., K+ currents activated by leukotriene D-4 or osmotic swelling in Ehrlich ascites tumour cells, PFLUG ARCH, 440(2), 2000, pp. 283-294
K+ and Cl- currents activated by hypoosmotic cell swelling (I-K,I-vol and I
-Cl,I-vol) or after addition of leukotriene D-4 (LTD4) to cells in isotonic
medium were studied in Ehrlich ascites tumour cells. I-K,I-vol and I-Cl,I-
vol were not affected by strong buffering of intracellular Ca2+ or by addit
ional removal of extracellular Ca2+. In isotonic media, 5 nmol/l LTD4 activ
ated large K+ but not Cl- cur rents. The LTD4-activated I-K was, as has bee
n shown previously for I-K,I-vol, insensitive to charybdotoxin (ChTX) but w
as blocked by the antiarrhythmic drug clofilium. The current/voltage (I/V)
relation for the LTD4-activated I-K was, as recently demonstrated for I-K,I
-vol, well fitted by the Goldman-Hodgkin-Katz current equation between -130
mV and 30 mV in both physiological and K+-rich extracellular solutions. LT
D4 had no additional effect on the magnitude of I-K in Ehrlich cells alread
y activated by the hypoosmotic stimulus. Nevertheless, the onset time for I
-K after hypoosmotic cell swelling was significantly less in the presence o
f LTD4. The similar I/V relation, pharmacological sensitivity and lack of a
dditivity suggest that hypoosmotic swelling and addition of LTD4 activate t
he same K+ channels in Ehrlich cells. The influence of [Ca2+](i) appears, h
owever, to differ between I-K,I-vol and the I-K activated by LTD4 in that t
he latter was reduced significantly by strong buffering of [Ca2+](i). This
might reflect the involvement of some additional factor in the hypoosmotic
activation of K+ channels besides the stimulation mediated by LTD4.