| Literature DB >> 12865316 |
Tomoko Chiyo1, Takeshi Yamazaki, Kenji Aoshika, Shiro Kominami, Yoshihiro Ohta.
Abstract
The rapid effects of steroid hormones on Ca(2+) signals have been examined in bovine adrenocortical cells. Among the steroid molecules tested, only corticosterone rapidly stimulated Ca(2+) signals upon addition of ACTH, although corticosterone alone did not induce Ca(2+) signals. Corticosterone also enhanced steroidogenesis induced by ACTH. The enhancement of ACTH-induced Ca(2+) signals was also observed with membrane-impermeable corticosterone conjugated to BSA and was not inhibited by cycloheximide. In addition, corticosterone did not enhance Ca(2+) signals induced by ATP or angiotensin II. These results suggest that corticosterone selectively stimulates ACTH-induced Ca(2+) signals in a nongenomic way by acting on a target in the plasma membrane. Furthermore, the supernatants of cells incubated with ACTH or ATP enhanced Ca(2+) signals, suggesting that steroids produced by such treatment act in an autocrine fashion. Consistent with this idea, these effects were inhibited by inhibitors of steroidogenesis (aminoglutethimide or metyrapone). These results show that steroid molecules synthesized in adrenocortical cells facilitate ACTH-induced Ca(2+) signals. Taken together, corticosterone secreted from adrenocortical cells activates ACTH-induced Ca(2+) signals and steroidogenesis by nongenomic means.Entities:
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Year: 2003 PMID: 12865316 DOI: 10.1210/en.2002-221126
Source DB: PubMed Journal: Endocrinology ISSN: 0013-7227 Impact factor: 4.736