Document Detail

Angiotensin II (AII) and adrenocorticotropin release: modulation by estradiol of the AII biological activity and binding characteristics in anterior pituitary dispersed cells.
MedLine Citation:
PMID:  2838267     Owner:  NLM     Status:  MEDLINE    
The present studies were designed to test if estrogens influence basal and angiotensin II (AII)-stimulated ACTH release and the binding characteristics of AII receptors in isolated anterior pituitary (AP) cells from estrogen-deplete and estrogen-replete rats incubated in vitro. AP cells were obtained from various adult donors: randomly cycling (rc), 10-day ovariectomized (Ovx), Ovx with estradiol restored at a circulating physiological level (Ovx + lEB), Ovx with estradiol at a supraphysiological circulating level (Ovx + hEB); and male (m) rats. The amount of ACTH released under basal conditions was similar in the rc, Ovx + lEB, and m groups, although this amount was significantly greater (P less than 0.02) than that in the Ovx and Ovx + hEB groups. The ACTH-releasing activity (CRA) of AII was concentration dependent (10(-9)-10(-6) M) in all cells. The rank order of the CRA of AII in the groups varied as follows: rc = Ovx + lEB greater than Ovx = Ovx + hEB = m. The slopes of the AII responses were similar. Estradiol addition in vitro did not modify either basal or AII-stimulated ACTH release in any group of cells. AII binding studies indicated that AP cells from donors with different circulating estradiol levels had similar apparent equilibrium dissociation constants (Kd, 16-30 nM). However, the maximum binding capacities in AP cells from the m, Ovx, and Ovx + hEB groups (40, 51, and 49 fmol/10(6) cells, respectively) were significantly lower (P less than 0.05) than those in the rc and Ovx + lEB groups (77 and 81 fmol/10(6) cells, respectively). In summary, these studies indicate that 1) circulating levels of estradiol are able to modulate spontaneous ACTH release by dispersed AP cells; and 2) circulating estradiol, at a lower or higher level than that during the estrous cycle, decreases the in vitro ACTH-releasing activity of AII, possibly through a reduction in the number of AP AII receptors. These results further suggest that estrogen is likely to have a physiological role in corticotropic function.
E Spinedi; L Herrera; A Chisari
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Endocrinology     Volume:  123     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1988 Jul 
Date Detail:
Created Date:  1988-07-29     Completed Date:  1988-07-29     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  641-6     Citation Subset:  AIM; IM    
Centro de Referencia de Radioinmunoensayo, La Plata, Argentina.
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MeSH Terms
Adrenocorticotropic Hormone / secretion*
Angiotensin II / metabolism,  pharmacology*
Cells, Cultured
Estradiol / pharmacology*
Pituitary Gland, Anterior / drug effects,  metabolism*
Rats, Inbred Strains
Receptors, Angiotensin / drug effects,  metabolism*
Reference Values
Reg. No./Substance:
0/Receptors, Angiotensin; 11128-99-7/Angiotensin II; 50-28-2/Estradiol; 9002-60-2/Adrenocorticotropic Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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