Evidence for two independent pathways in the stimulation of steroidogenesis by luteinizing hormone involving chloride channels and cyclic AMP.
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 (less than or equal to 1 ng/ml), but not at high (100 ng/ml) 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.
Choi
M S
MS
Department of Biochemistry, Royal Free Hospital School of Medicine, University of London, England.
Cooke
B A
BA
D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D018118:Chloride Channels; D002712:Chlorides / Q000502:physiology*; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000502:physiology*; D007985:Leydig Cells / Q000187:drug effects / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000494:pharmacology*; D008297:Male; D008565:Membrane Proteins / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013739:Testosterone / Q000096:biosynthesis*
D018118:Chloride Channels; D002712:Chlorides; D008565:Membrane Proteins; D005576:Colforsin; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D013739:Testosterone; D003994:Bucladesine; D007986:Luteinizing Hormone; D000242:Cyclic AMP