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Evidence for two independent pathways in the stimulation of steroidogenesis by luteinizing hormone involving chloride channels and cyclic AMP
Author(s) -
Choi Michael S.K.,
A. Cooke Brian
Publication year - 1990
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(90)80602-f
Subject(s) - endocrinology , medicine , forskolin , luteinizing hormone , chemistry , stimulation , chloride , chloride channel , extracellular , hormone , biology , biochemistry , organic chemistry
The possible role of chloride channels in luteinizing hormone (LH) action on steroidogenesis in rat Leydig cells had been investigated. A chloride channel blocker, SITS (4‐acetamido‐4'‐isothiocyanatostilbene‐2,2'‐disulphonic acid), inhibited LH‐stimulated steroidogenesis at low (⩽ 1), but not at high (100) LH concentrations. In addition, dibutyryl cyclic AMP‐ and forskolin‐stimulated steroidogenesis was unaffected by SITS. The removal of extracellular chloride potentiated steroidogenesis stimulated by submaximal but not maximal doses of LH. These results suggest that at low levels of LH, steroidogenesis depends on chloride channels whereas with high levels, cyclic AMP is the mediator of LH action.