In vitro effect of cytochalasin B on adrenal steroidogenesis in frog.
In order to examine the role of microfilaments in adrenal steroidogenesis, we have studied the effect of cytochalasin B on corticosteroid secretion by frog interrenal tissue in vitro. Perifusion of interrenal fragments with increasing concentrations of cytochalasin B (ranging from 10(-8) to 10(-4) M) led to a dose-related inhibition of corticosterone and aldosterone secretion. Immunohistochemical examination of adrenocortical fragments, using specific anti-actin antibodies, showed that cytochalasin B (5 X 10(-5) M) was responsible for the disappearance of the microfilament network. Administration of 2 consecutive doses of cytochalasin B (5 X 10(-5) M) was responsible for a reproducible and reversible inhibition of corticosteroid secretion. In addition, cytochalasin B (5 X 10(-5) M) totally inhibited the stimulatory effect of angiotensin II, prostaglandin E1 and VIP. It also induced a marked decrease in both ACTH- and dbcAMP-induced stimulation of corticosteroidogenesis. These data indicate that cytochalasin B, which blocked the effect of all adrenal stimulating factors tested, interferes with a late step in the common pathway involved in the response of frog adrenocortical cells to all corticotropic stimuli.
D008841:Actin Cytoskeleton / Q000187:drug effects / Q000502:physiology; D000302:Adrenal Cortex / Q000378:metabolism*; D000305:Adrenal Cortex Hormones / Q000096:biosynthesis*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000037:antagonists & inhibitors; D003571:Cytochalasin B / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D011898:Ranidae; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology
D000305:Adrenal Cortex Hormones; D000451:Mineralocorticoid Receptor Antagonists; D000804:Angiotensin II; D014660:Vasoactive Intestinal Peptide; D003571:Cytochalasin B; D003345:Corticosterone