Effect of 17β-Estradiol on Somatostatin Receptor Expression and Inhibitory Effects on Growth Hormone and Prolactin Release in Rat Pituitary Cell Cultures

• Published in: Endocrinology (Philadelphia) Vol. 139; no. 5; pp. 2272 - 2277
• Main Authors: Djordjijevic, D, Zhang, J, Priam, M, Viollet, C, Gourdji, D, Kordon, C, Epelbaum, J
• Format: Journal Article
• Language: English
• Published: Washington Endocrine Society 01-05-1998; Oxford University Press
• Subjects: 17β-Estradiol; Accumulation; Agonists; Cyclic AMP; Females; Gene expression; Growth hormones; Octreotide; Pituitary; Prolactin; Receptors; Secretion; Sex hormones; Somatostatin; Somatostatin receptors; Up-regulation
• ISSN: 0013-7227; 1945-7170
• DOI: 10.1210/endo.139.5.5990

In the present study, we tested whether 17β-estradiol
(E2)-induced PRL sensitivity to somatostatin-14 (SRIF)
involves selective up-regulation of discrete somatostatin receptor
subtypes (ssts) in primary cultures of female rat pituitary cells. The
efficacy of the endogenous peptide SRIF to inhibit GH and PRL secretion
and cAMP accumulation was compared with those of octreotide (OCT),
BIM-23052, BIM-23056, and BIM-23268, which have been reported to be
relatively selective for rat sst2, sst3, and sst5. Experiments were
performed in steroid-depleted media supplemented or not with 1
nm E2 for 96 h. SRIF, OCT, and BIM-23052
inhibited cAMP accumulation and GH release independently of
E2. In contrast, all three agonists affected PRL release in
E2-treated cultures only. Inhibition of cAMP accumulation
by SRIF, OCT, and BIM-23052 was enhanced by exposure of cells to
E2. The rank of potency of the agonists, OCT =
SRIF > BIM-23052, was similar for GH and PRL inhibition.
BIM-23268 was a weak agonist on GH, but not on PRL, secretion.
BIM-23056 had no effect on the release of either hormone, but slightly
inhibited cAMP formation in E2-treated cells. To verify
whether SRIF receptor gene expression correlated with these
observations, messenger RNA (mRNA) transcripts corresponding to the
five ssts were measured by quantitative RT-PCR in the presence or
absence of E2. Control cells expressed predominantly sst2
and sst3 transcripts; sstl mRNA was present in moderate amounts,
whereas sst4 and sst5 were only weakly expressed. E2 had a
differential effect on distinct ssts; it increased mRNA concentrations
corresponding to sst2 and sst3, and decreased that of sst1. These
results indicate that sst2 and sst3 receptors are the major
somatostatin receptors expressed in the female rat pituitary, and that
both of them are positively regulated by estradiol. However, the
capacity of lactotropes to respond to SRIF after exposure to
E2 seems to depend more upon E2-induced
up-regulation of the sst2 than of the sst3 receptor subtype.