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PAUL M. PLOTSKY, WYLIE VALE, Hemorrhage-Induced Secretion of Corticotropin-Releasing Factor-Like Immunoreactivity into the Rat Hypophysial Portal Circulation and Its Inhibition by Glucocorticoids, Endocrinology, Volume 114, Issue 1, 1 January 1984, Pages 164–169, https://doi.org/10.1210/endo-114-1-164
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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. (Endocrinology114: 164, 1984)
