K+ currents activated by leukotriene D-4 or osmotic swelling in Ehrlich ascites tumour cells

Citation
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
Citations number
34
Categorie Soggetti
Physiology
Journal title
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
ISSN journal
00316768 → ACNP
Volume
440
Issue
2
Year of publication
2000
Pages
283 - 294
Database
ISI
SICI code
0031-6768(200006)440:2<283:KCABLD>2.0.ZU;2-4
Abstract
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.