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This version published online on October 30, 2003
Endocrinology, doi:10.1210/en.2003-1222
A more recent version of this article appeared on January 1, 2004
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Submitted on September 15, 2003
Accepted on October 22, 2003

Possible Involvement of Ryanodine Receptor-Mediated Intracellular Calcium Release in the Effect of Corticotropin-Releasing Factor on Adrenocorticotropin Secretion

ETSUKO YAMAMORI1, YASUMASA IWASAKI1*, YUTAKA OKI1, MASANORI YOSHIDA1, MASATO ASAI1, MACHIKO KAMBAYASHII1, YUTAKA OISO1, and NOBUO NAKASHIMA1

1 Departments of Medicine (E.Y., M.Y., M.A., Y.O.) and Clinical Pathophysiology (Y.I., M.K., N.N.), Nagoya University Graduate School of Medicine and Hospital, Nagoya 466-8550, Department of Medicine II (Y.O.), Hamamatsu University School of Medicine, Hamamatsu 431-3192; Japan

* To whom correspondence should be addressed. E-mail: iwasakiy{at}med.nagoya-u.ac.jp.

We examined the role of intracellular calcium release in the regulation of CRH-induced ACTH secretion using the AtT20 corticotroph cell line. We found that ruthenium red, an inhibitor of ryanodine receptor, substantially diminished the secretory response, whereas Xestospongin C, an IP3 receptor antagonist, had no effect. Expression of two ryanodine receptor subtypes (RyR1 and RyR3) was confirmed by RT-PCR. We also found that caffeine, a ryanodine receptor agonist, significantly stimulated, whereas thapsigargin, which causes depletion of intracellular calcium store, markedly diminished, the ACTH release. These results suggest that ryanodine receptor-mediated calcium-induced calcium release is involved in the regulation of CRH-induced ACTH release.
Key words: ryanodine receptor • CRH • ACTH • calcium • corticotroph




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S. M. Soares, M. Thompson, and E. N. Chini
Role of the Second-Messenger Cyclic-Adenosine 5'-Diphosphate-Ribose on Adrenocorticotropin Secretion from Pituitary Cells
Endocrinology, May 1, 2005; 146(5): 2186 - 2192.
[Abstract] [Full Text] [PDF]


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