Relative and combined effects of estradiol and prolactin on corticosterone secretion in ovariectomized rats.
In vivo and in vitro experiments were designed to assess the relationship of the estradiol (E2) and prolactin (PRL) on glucocorticoid secretion in ovariectomized (Ovx) rats. Female rats were Ovx for two weeks and then subcutaneously injected with oil or estradiol benzoate (EB) for 3 days before experimentation. Venous blood samples were collected from right jugular vein at 0, 30, 60, 90, and 120 min after challenge with adrenocorticotropin (ACTH). Adrenal zona fasciculata-reticularis (ZFR) cells from Ovx rats were isolated and incubated with E2 or PRL. In the morning and afternoon, EB enhanced the basal and ACTH-stimulated concentrations of plasma corticosterone (CORT) and PRL. Administration of E2 in vitro increased the basal and ACTH-stimulated release of CORT and production of adenosine 3', 5'-cyclic monophosphate (cAMP) in ZFR cells. E2 enhanced the forskolin-stimulated release of CORT by ZFR cells. However, the 3-isobutyl-l-methylxanthine (IBMX)- or 8-Br-cAMP-stimulated release of CORT was not affected by E2. E2 augmented the lower doses of PRL-stimulated release of CORT and cAMP accumulation as compared with the PRL-treated group alone. Incubation of higher doses of PRL increased the production of cAMP. Administration of nifedipine and R(+) BK8644 (classic L-type Ca2+ channel blocker) significantly attenuated the PRL-stimulated release of CORT. Taken together, these data indicate that E2- and PRL-related increase of CORT in Ovx rats is associated with the increase of cAMP accumulation and calcium influx in ZFR cells. In conclusion, E2 and PRL play a stimulatory role in the co-regulation of CORT secretion.
Lo
Ming-Jae
MJ
Department of Physical Therapy, Hungkuang University, Taichung 433, Taiwan, Republic of China. lo@sunrise.hk.edu.tw
Wang
Paulus S
PS
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000378:metabolism; D005576:Colforsin / Q000494:pharmacology; D003345:Corticosterone / Q000097:blood / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D004357:Drug Synergism; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D007275:Injections, Intravenous; D009543:Nifedipine / Q000494:pharmacology; D010052:Ovariectomy; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011388:Prolactin / Q000097:blood / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects
D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D010726:Phosphodiesterase Inhibitors; D005576:Colforsin; D015124:8-Bromo Cyclic Adenosine Monophosphate; D004958:Estradiol; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D000242:Cyclic AMP; D009543:Nifedipine; D015056:1-Methyl-3-isobutylxanthine; D003345:Corticosterone