The effects of pineal indoles and a crude aqueous pineal extract on ACTH mediated corticosterone release by isolated adrenal cells

Life Sciences ◽  
1977 ◽  
Vol 20 (8) ◽  
pp. 1363-1371 ◽  
Author(s):  
Johnny R. Porter ◽  
Mark Heiman
2004 ◽  
pp. 613-618 ◽  
Author(s):  
AY Shevchenko ◽  
NM Bazhan ◽  
EN Makarova ◽  
TV Yakovleva ◽  
NR Karkaeva

OBJECTIVE: The antagonism of Agouti protein (AP) and Agouti-related protein on melanocortin receptors suggests an inhibitory role in the regulation of steroidogenesis. However, we have previously demonstrated that ectopic AP overexpression increased restraint-induced corticosterone release and adrenal reactivity to ACTH in mice. A high steroidogenic response to ACTH may be a consequence of a stimulatory AP action on the adenylate cyclase (AC) and/or intracellular steroidogenic enzymes. The aim of the present study was to estimate the effect of ectopic AP overexpression on the activity of AC and steroidogenic intracellular enzymes. METHODS: ACTH and forskolin were used for AC stimulation, and dibutyryl cAMP and progesterone were used for stimulation of intracellular steroidogenic enzymes in isolated adrenal cells in male C57Bl/6J mice of two Agouti genotypes: A(y)/a (ectopic AP overexpression) and a/a (absence of AP in all tissues). RESULTS: ACTH and forskolin increased cAMP accumulation to the same extent in both A(y)/a and a/a mouse adrenal cells (P<0.001; ANOVA), but resulted in higher corticosterone production in A(y)/a mice (P<0.001 for ACTH and P<0.01 for forskolin; ANOVA). Dibutyryl cAMP- and progesterone-induced corticosterone production was higher in A(y)/a mice than in a/a mice (P<0.001 for dibutyryl cAMP and P<0.01 for progesterone; ANOVA). CONCLUSIONS: Ectopic AP overexpression increased stimulated corticosterone production and intracellular steroidogenic enzyme reactivity to cAMP without an effect on AC activity.


1992 ◽  
Vol 263 (3) ◽  
pp. E461-E466 ◽  
Author(s):  
A. R. Gwosdow ◽  
N. A. O'Connell ◽  
J. A. Spencer ◽  
M. S. Kumar ◽  
R. K. Agarwal ◽  
...  

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)


1972 ◽  
Vol 18 (2) ◽  
pp. 372-377 ◽  
Author(s):  
Mary K. Vaughan ◽  
Russel J. Reiter ◽  
George M. Vaughan ◽  
Lewellyn Bigelow ◽  
Mark D. Altschule

2014 ◽  
Author(s):  
Somrudee Saiyudthong ◽  
Sirinun Pongmayteegul ◽  
Udomsri Showpittapornchai ◽  
Pansiri Phansuwan-Pujito

2021 ◽  
Vol 526 ◽  
pp. 111195
Author(s):  
Daniel P. Fudulu ◽  
George Horn ◽  
Georgina Hazell ◽  
Anne-Marie Lefrançois-Martinez ◽  
Antoine Martinez ◽  
...  

1983 ◽  
Vol 97 (3) ◽  
pp. 357-367 ◽  
Author(s):  
Andrew Baird ◽  
K. W. Kan ◽  
Samuel Solomon

Synthetic (1–39)ACTH, (1–24)ACTH, (18–39)ACTH, α-MSH, met-enkephalin and α-, βand γ-endorphin were tested for their ability to stimulate steroidogenesis by human fetal adrenal cells in culture. Adrenal cells were incubated with peptide hormones for two periods of 24 h. On the third day of the experiment the cells were incubated with progesterone (4 μg/2 ml) for 8 h. At the doses tested only (1–39)ACTH, (1–24)ACTH and α-MSH stimulated steroidogenesis. None of the other peptides had any corticotrophic effect on the formation of cortisol, corticosterone or dehydroepiandrosterone sulphate (DHAS). At the highest doses tested, α-MSH (100 μg/2 ml) had a corticotrophic effect that was not different from that obtained with 20 ng (1–39)ACTH or (1–24)ACTH. At the lower doses (0·2–2 μg/2 ml), α-MSH stimulated the formation of DHAS (P<0·01) without stimulating the formation of cortisol.


1989 ◽  
Vol 264 (12) ◽  
pp. 6858-6862
Author(s):  
A Penhoat ◽  
D Naville ◽  
C Jaillard ◽  
P G Chatelain ◽  
J M Saez

1971 ◽  
Vol 44 (4) ◽  
pp. 898-904 ◽  
Author(s):  
Abbas E. Kitabchi ◽  
Donald B. Wilson ◽  
Rameshwar K. Sharma ◽  
Louise C. Kitchell
Keyword(s):  

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