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In the Rat, Interleukin- l and -β Stimulate Adrenocorticotropin and Catecholamine Release^*

CATHERINE RIVIER, WYLIE VALE and MARVIN BROWN

The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute La Jolla, California 92037
the Department of Medicine University of California Medical Center San Diego, California 92103–9981

Address all correspondence and requests for reprints to: Dr. Catherine Rivier, The Salk Institute, P.O. Box 85800, 10010 North Torrey Pines Road, La Jolla, California 92037.

Abstract

Recombinant interleukin-l and-β (Il-1 and - β) have been evaluated for their abilities to stimulate ACTH and catecholamine secretion in the intact adult male rat. Additionally, the role of adrenergic-dependent pathways in mediating Il-1-induced ACTH release has been assessed. The iv or intracerebroventricular injection of either II-l or 11–1β caused doserelated increases in plasma ACTH, epinephrine, and norepinephrine levels. While at low iv doses (10 ng), 11–1β was more effective than Il-l at releasing ACTH, no measurable differences were noted at higher doses. In contrast, 11–1β was significantly more active at all doses in elevating plasma ACTH levels after intracerebroventricular injection. Similarly, Il-l was more effective than 11–1β at stimulating epinephrine, but not norepinephrine, secretion after icv injection. Because of the ability of catecholamines to alter ACTH secretion, we then examined the role of adrenergic-dependent pathways as possible mediators of Il-1-induced ACTH secretion. Blockade of adrenergic receptors by the concomitant administration of prazosin and propanolol prevented the simultaneous actions of phenylephrine and isoproterenol on the corticotrophs, but did not significantly alter the effect of peripherally administered Il-l on ACTH release.

These results suggest that both Il-l and 11–1β stimulate ACTH and catecholamine secretion in the rat. Despite the ability of the lymphokine to elevate plasma epinephrine and norepinephrine values, circulating catecholamines do not appear to represent essential modulators of ACTH release induced by acutely injected 11–1.

Footnotes

^* This work was supported by NIH Grants DK-26741 and HL-37716 and was conducted in part by the Clayton Foundation for Research, California Division.

Clayton Foundation Investigator.

Received May 22, 1989.

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