Involvement of the cytoskeleton in the mechanism of action of endothelin on frog adrenocortical cells.
In a previous report, we have shown that endothelin-1 (ET-1) is a potent stimulator of corticosterone and aldosterone secretion by frog adrenocortical cells. In the present study, we examine the possible involvement of cytoskeletal elements in the mechanism of action of ET-1 on corticosteroid secretion from frog adrenal gland. The microfilament disrupting agent cytochalasin B (5 x 10(-5) M) induced a reversible inhibition of the spontaneous secretion of corticosteroid and blocked the response of adrenocortical cells to ET-1 (5 x 10(-9) M). In contrast, the antimicrotubular agent vinblastine (10(-5) M) and the intermediate filament inhibitor beta-beta' iminodipropionitrile (10(-3) M) had virtually no effect on both spontaneous and endothelin-induced steroidogenesis. Taken together, these results indicate that, in the frog adrenal gland, the integrity of the microfilament network is required for the corticotropic activity of ET-1 whereas microtubules and intermediate filaments are apparently not involved in the mechanism of action of ET-1.
Remy-Jouet
I
I
European Institute for Peptide Research, Laboratory of Cellular and Molecular Neuroendocrinology, INSERM 4413, UA CNRS, University of Rouen, Mont-Saint-Aignan, France.
Delarue
C
C
Feuilloley
M
M
Vaudry
H
H
D000302:Adrenal Cortex / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D002478:Cells, Cultured; D003571:Cytochalasin B / Q000494:pharmacology; D003599:Cytoskeleton / Q000378:metabolism*; D016232:Endothelins / Q000494:pharmacology*; D008297:Male; D009570:Nitriles / Q000494:pharmacology; D011895:Rana ridibunda; D014747:Vinblastine / Q000494:pharmacology
D016232:Endothelins; D009570:Nitriles; D003571:Cytochalasin B; C008110:3,3'-iminodipropionitrile; D014747:Vinblastine