HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cam, G. R. Articles by Bassett, J. R. Search for Related Content PubMed Articles by Cam, G. R. Articles by Bassett, J. R.

The intraperitoneal injection of (1–24)ACTH (34–170 nmol/kg) in rats pretreated with betamethasone resulted in a biphasic rise in plasma corticosterone; only a single phase-response was observed after lower doses (3·4–17·0 nmol/kg). There was an initial rapid rise to a level of approximately 0·72 µmol corticosterone/l plasma over the first 10 min after injection, followed by a plateau phase in which there was no further significant rise in steroid levels up to 25 min. Between 25 and 30 min after injection there was a second significant rise in plasma corticosterone concentration. The amplitude of the first phase of steroid increase was essentially the same for all doses of (1–24)ACTH administered whereas the amplitude of the second phase was dose-dependent. The administration of the microtubule inhibitor, colchicine, greatly reduced the amplitude of the second phase of the response to (1–24)ACTH while not affecting the first phase. However, a second stimulus with (1–24)ACTH in colchicine-treated animals was without effect on plasma corticosterone concentrations; both the first and second phases of corticosteroid increase being abolished. It is proposed that the first phase of plasma corticosterone increase resulted from the release of corticosteroid from a storage form close to the cell membrane and not requiring microtubular transport, whereas the second phase was the result of transport from more distant storage sites or de-novo synthesis.

This article has been cited by other articles:

				C. H Brennan, A. Chittka, S. Barker, and G. P Vinson Eph receptors and zonation in the rat adrenal cortex J. Endocrinol., July 1, 2008; 198(1): 185 - 191. [Abstract] [Full Text] [PDF]

				P. M. Jamieson, C. Li, C. Kukura, J. Vaughan, and W. Vale Urocortin 3 Modulates the Neuroendocrine Stress Response and Is Regulated in Rat Amygdala and Hypothalamus by Stress and Glucocorticoids Endocrinology, October 1, 2006; 147(10): 4578 - 4588. [Abstract] [Full Text] [PDF]