AJP - Endocrinology and Metabolism, Vol 263, Issue 3 E461-E466, Copyright © 1992 by American Physiological Society
Interleukin-1-induced corticosterone release occurs by an adrenergic mechanism from rat adrenal gland
A. R. Gwosdow, N. A. O'Connell, J. A. Spencer, M. S. Kumar, R. K. Agarwal, H. H. Bode and A. B. Abou-Samra
Endocrine Unit of Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Interleukin-1 (IL-1) has been shown to stimulate corticosterone release
from the adrenal gland directly, and indirectly through activation of the
hypothalamic-pituitary-adrenal axis. The aim of this paper was to determine
whether IL-1-stimulated corticosterone release occurs indirectly through
the local release of catecholamines from the rat adrenal gland. To
accomplish this, experiments were conducted on both quartered rat adrenal
glands and primary cultures of dispersed adrenal cells. Incubation of
quartered adrenals with adrenocorticotropic hormone (ACTH, 10(-12) to
10(-8) M) or IL-1 beta (10(-12) to 10(-8) M) resulted in dose-dependent
increases (P less than 0.05) in corticosterone release. Corticosterone
release stimulated by 10(-8) M doses of ACTH and IL-1 beta began to rise 30
min after incubation and peaked at 2 h. In primary cultures of adrenal
cells, IL-1 alpha and IL-1 beta elevated corticosterone release after a
24-h incubation period. ACTH elevated corticosterone levels at 4 and 24 h.
The stimulatory effect of IL-1 on corticosterone release was mimicked by
epinephrine (10(-6) M), and was selectively blocked by the alpha-adrenergic
antagonist phentolamine (10(-5) M). The beta-adrenergic antagonist
propranolol (10(-5) M) did not change IL-1-induced corticosterone release.
Neither phentolamine nor propranolol had an effect on ACTH-stimulated
corticosterone release. Both IL-1 alpha and IL-1 beta significantly
increased (P less than 0.05) epinephrine levels after a 24-h incubation
period compared with media-treated controls.(ABSTRACT TRUNCATED AT 250
WORDS)
