AJP - Endocrinology and Metabolism, Vol 243, Issue 2 109-E113, Copyright © 1982 by American Physiological Society
Estradiol stimulation of pituitary cAMP production and cAMP binding
L. K. Tang, A. C. Martellock and F. Y. Tang
The role of 17 beta-estradiol (E2) in the modulation of N6,O2'-dibutyryl
adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced hormone release was
examined in pituitary monolayer cultures prepared from intact and
ovariectomized female rats. Incubations with 5 mM DBcAMP for 4 h
significantly (P less than 0.05) stimulated both luteinizing hormone (LH)
and prolactin (PRL) release in pituitary cultures prepared from rats at
diestrus and from cycling rats at random stages of the estrous cycle.
However, DBcAMP failed to stimulate the LH or PRL release in cultures
prepared from ovariectomized rats in which the basal LH and PRL release was
approximately three-fold and one-tenth of that in cycling rats,
respectively. Pretreatment with 1 nM E2 augmented or restored the
DBcAMP-induced LH release but not the DBcAMP-induced PRL release in
cultures prepared from cycling or ovariectomized rats, respectively.
Furthermore, E2 treatment alone of cultures prepared from cycling rats
significantly increased intracellular cAMP concentrations and cAMP-binding
activities by at least twofold over that of the non-E2-treated controls.
The E2-induced rise in cellular cAMP concentration preceded the E2-induced
rise in cAMP binding. These results indicate that the priming effect of E2
on pituitary LH responsiveness to DBcAMP is associated with increased cAMP
production and cAMP binding.
