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Endocrinology, doi:10.1210/endo-114-1-164
Endocrinology Vol. 114, No. 1 164-169
Copyright © 1984 by the Endocrine Society.
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Hemorrhage-Induced Secretion of Corticotropin-Releasing Factor-Like Immunoreactivity into the Rat Hypophysial Portal Circulation and Its Inhibition by Glucocorticoids*

PAUL M. PLOTSKY and WYLIE VALE{dagger}

Peptide Biology Laboratory, The Salk Institute San Diego, California 92138

Address requests for reprints to: Dr. Paul M. Plotsky, Peptide Biology Laboratory, The Salk Institute, P.O. Box 85800, San Diego, California 92138.

Abstract

A paradigm for reliably stimulating ACTH secretion in urethane-anesthetized male rats has been used to examine hypothalamic secretion of corticotropin-releasing factor- like immunoreactivity (CRF-LI) into the hypophysial portal circulation. Hemorrhage of 15% estimated blood volume evoked a maximal 4.6-fold elevation in circulating ACTH levels from an initial level of 178.4 ± 51.2 (±SE) to 814.7 ± 184.6 pg ml–1. The cumulative amount of ACTH secreted in response to hemorrhage was 10-fold greater than the cumulative amount of ACTH secreted by nonhemorrhaged rats (unweighted cumulative effect over all time points).

In another experiment from a similarly hemorrhaged group, the hypophysial portal plasma CRF-LI concentration rose 2-fold from an initial level of 429.7 ± 34.2 to 839.3 ± 170.4 pg ml–1. Pretreatment with dexamethasone (100 µg/kg BW, im) had no effect on initial levels of either CRF-LI or ACTH. The hemorrhage- induced elevations of both CRF-LI and ACTH were abolished in dexamethasone-treated rats.

The secretory rate of CRF-LI was calculated to be 1.61 ± 0.7 pg min–1 in nonhemorrhaged animals. Reversible pharmacological hyperpolarization of the paraventricular nuclei by stereotaxically microinjected procaine (15 µg/100 nl) reduced portal plasma CRF-LI and peripheral plasma ACTH to undetectable levels.

These observations led to the following conclusions: 1) CRFLI is an important hypothalamic regulator of adenohypophysial ACTH secretion, 2) CRF-LI in the hypophysial portal circulation is derived from CRF-LI-containing neurons within the paraventricular nuclei, and 3) glucocorticoid negative feedback effects can be exerted at the central level. (Endocrinology 114: 164, 1984)

Footnotes

* Presented in part of the 65th Annual Meeting of The Endocrine Society, San Antonio, TX, 1983. This work was supported in part by NIH Grant AM-26741 and a grant from the Mellon Foundation (to P.M.P.). Research was conducted in part by The Clayton Foundation for Research, California Division.

{dagger} Investigator, Clayton Foundation.

Received April 25, 1983.




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