help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Minamitani, N.
Right arrow Articles by Fujita, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Minamitani, N.
Right arrow Articles by Fujita, T.

Endocrinology, Vol 117, 347-353, Copyright © 1985 by Endocrine Society

ARTICLES

Inhibitory effect of [Asu1,7]-eel calcitonin on growth hormone- secretion in conscious, freely moving, male rats

N Minamitani, K Chihara, H Kaji, H Kodama and T Fujita

The effect of [Asu1,7]-eel calcitonin (ECT), which is an equipotent analog of eel calcitonin (CT), on GH secretion was investigated in freely moving conscious male rats. Pulsatile GH secretion was completely inhibited by iv injection of ECT (2.5 micrograms/rat). The mean 6-h plasma GH levels, 9.54 +/- 2.34 ng/ml (mean +/- SEM) in ECT- treated rats, were significantly lower than those in saline-treated rats (69.9 +/- 9.4 ng/ml, P less than 0.001). In order to examine the action of ECT on the central nervous system, 25 ng ECT dissolved in 10 microliters saline were injected into the lateral ventricle of conscious male rats. The bursts of GH secretion were completely abolished by this dose of intraventricularly (ivt) injected ECT. The mean 6-h GH levels 5.8 +/- 0.8 ng/ml, were also significantly lower than those in control rats (35.8 +/- 6.6 ng/ml, P less than 0.01). Serum Ca levels did not change after the ivt injection of 25 ng ECT but fell significantly after the iv injection of 2.5 micrograms ECT. In order to clarify the inhibitory mechanism of GH secretion by ECT, the effect of ECT on the release of GH elicited by prostaglandin E1 (PGE1), a well-known GH secretagogue acting directly on the pituitary, was examined in vivo as well as in vitro. Both ivt (2.5, 25, or 250 ng/10 microliters X rat) and iv (2.5 or 25 micrograms/rat) injections of ECT caused a significant and dose-dependent suppression of PGE1-induced GH rises in conscious rats. In contrast, 10(-8) to 10(-7) M ECT failed to affect the baseline secretion of GH and its release by 5 X 10(-6) M PGE1 from rat anterior pituitary tissues perifused in vitro. These findings suggest that ECT suppresses GH secretion in the rat, at least in part, through the central nervous system.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
S.-C. Tsai, C.-C. Lu, J.-J. Chen, Y.-C. Chiao, S.-W. Wang, J.-J. Hwang, and P. S. Wang
Inhibition of salmon calcitonin on secretion of progesterone and GnRH-stimulated pituitary luteinizing hormone
Am J Physiol Endocrinol Metab, July 1, 1999; 277(1): E49 - E55.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1985 by The Endocrine Society