High local GH-releasing hormone (GHRH) levels are capable of inducing trans
differentiation in salivary cells to synthesize GH. Hoc-ever, the factors i
mplicated in this process remain unknown. To study this subject, normal and
Ames dwarf mice were implanted in the submaxillary gland with a slow relea
se pellet releasing 21 mug GHRH (1-29)-NH2/day for 2 months. Control animal
s received placebo pellets at the same site. After 60 days, heart blood was
collected and submaxillary glands were removed. Circulating levels of GH a
nd IGF-I were significantly decreased (P <0.05) in dwarf mice in comparison
with controls, and GHRH treatment did not modify tither of these two param
eters. Controls carrying GHRH pellets showed a significantly higher GH cont
ent (P <0.05) in the submaxillary gland than the placebo-treated normal mic
e. There were no differences between the IGF-I concentrations of placebo- a
nd GHRH-treated salivary tissue from normal mice. Analysis of GH mRNA by RT
-PCR followed by Southern blot revealed that GH transcripts were present in
the salivary gland samples carrying the placebo pellets in both normal and
dwarf mice. The expression of GH was significantly (P <0.05) increased by
the GHRH pellets in salivary tissue from normal mice, but not in submaxilla
ry glands From dwarf mice. Pit-1 mRNA was not detected in the GHRH-treated
glands of normal and dwarf mice by RT-PCR or by Southern blot. Using these
highly sensitive methods, we have been able to detect the transcription of
both GH and Pit-1 in pituitaries from Pit-1-deficient Ames dwarf mice. The
present experiment demonstrates that salivary tissue synthesizes GH when it
is exposed to the influence of GHRH. Both basal and GHRH-induced salivary
GH expression appear to be independent of Pit-1.