K+ currents activated by leukotriene D-4 or osmotic swelling in Ehrlich ascites tumour cells
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 additional removal of extracellular Ca2+. In isotonic media, 5 nmol/l LTD4 activated large K+ but not Cl- cur rents. The LTD4-activated I-K was, as has been shown previously for I-K,I-vol, insensitive to charybdotoxin (ChTX) but was 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. LTD4 had no additional effect on the magnitude of I-K in Ehrlich cells already activated by the hypoosmotic stimulus. Nevertheless, the onset time for I-K after hypoosmotic cell swelling was significantly less in the presence of LTD4. The similar I/V relation, pharmacological sensitivity and lack of additivity suggest that hypoosmotic swelling and addition of LTD4 activate the same K+ channels in Ehrlich cells. The influence of [Ca2+](i) appears, however, to differ between I-K,I-vol and the I-K activated by LTD4 in that the 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.
Más información
Título según WOS: | K+ currents activated by leukotriene D-4 or osmotic swelling in Ehrlich ascites tumour cells |
Título de la Revista: | PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY |
Volumen: | 440 |
Número: | 2 |
Editorial: | Springer |
Fecha de publicación: | 2000 |
Página de inicio: | 283 |
Página final: | 294 |
Idioma: | English |
URL: | http://link.springer.com/10.1007/s004240000273 |
DOI: |
10.1007/s004240000273 |
Notas: | ISI |