AJP - Endocrinology and Metabolism, Vol 241, Issue 1 14-E21, Copyright © 1981 by American Physiological Society
Effects of GnRH and drugs that affect cAMP levels on LH synthesis and release
T. C. Liu, P. S. Wang and G. L. Jackson
We examined basal and gonadotropin-releasing hormone (GnRH)-stimulated
luteinizing hormone (LH) release and synthesis in response to drugs that
raise intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels.
Anterior pituitaries from ovariectomized rats were incubated with or
without drugs in the presence of GnRH and [3H]glucosamine. Neither
8-bromo-cAMP (8-Br-cAMP) (10 mM), cholera toxin (10 micrograms/ml), nor
phosphodiesterase inhibitors [theophylline, 2 and 8 mM;
3-isobutyl-1-methylxanthine (MIX), 0.2 mM] had any detectable effect on
release of immunoreactive LH (IR-LH) when used alone. However, 8-Br-cAMP
and the inhibitors potentiated (P less than 0.01) GnRH-induced release of
IR-LH. Total radiolabeled LH in the system was elevated (P less than 0.01)
by either GnRH, 8-Br-cAMP for cholera toxin, but reduced (P less than 0.01)
by 8 mM theophylline and unaffected by MIX or 2 mM theophylline. 8-Br-cAMP
did not alter the effect of GnRH on radiolabeled LH in the total system,
whereas MIX and 2 mM theophylline reduced (P less than 0.05) it. These
results suggest that 1) cAMP does not effect LH release directly, but may
interact with GnRH to potentiate it, 2) GnRH and cAMP have a similar mode
of action on LH glycosylation, and 3) phosphodiesterase inhibitors have
additional actions that interfere with LH glycosylation.
