Is cAMP the obligatory second messenger in the action of lutropin on Leydig cell steroidogenesis.
Two adenylate cyclase inhibitors: 9-(tetrahydro-2-furyl)adenine and 2'5'-dideoxyadenosine decreased cAMP levels in LH-stimulated immature rat Leydig cells by 20-40%, independent of the concentration of LH. Steroid production was not correlated with this decrease in cAMP, but was increased (146%). The phorbol ester 4 beta-phorbol-12-myristate-13-acetate stimulated steroidogenesis and the phosphorylation of a 17 kD and a 33 kD protein, which was also stimulated by LH, whereas the inactive phorbol ester 4 beta-phorbol-12,13-diacetate did not have any effects. Moreover, the Ca2+-channel blocker diltiazem inhibited LH effects, but had no direct effects on the cholesterol side chain cleavage enzyme. It is concluded that cAMP may not be the only second messenger in LH action, and that other second messenger systems are probably also involved.
Themmen
A P
AP
Hoogerbrugge
J W
JW
Rommerts
F F
FF
van der Molen
H J
HJ
D000067956:Adenylyl Cyclase Inhibitors; D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism*; D004110:Diltiazem / Q000494:pharmacology; D066298:In Vitro Techniques; D007985:Leydig Cells / Q000187:drug effects* / Q000378:metabolism; D007986:Luteinizing Hormone / Q000494:pharmacology*; D008297:Male; D010703:Phorbol Esters / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013256:Steroids / Q000096:biosynthesis*
D000067956:Adenylyl Cyclase Inhibitors; D010703:Phorbol Esters; D013256:Steroids; D007986:Luteinizing Hormone; D000242:Cyclic AMP; D004110:Diltiazem