INV SUPERIOR JUBILADO
SEILICOVICH Adriana
artículos
Título:
Role of phosphodiesterase and protein kinase-G in nitric oxide-induced inhibition of prolactin release from the rat anterior pituitary.
Autor/es:
M.O.VELARDEZ,; A. DE LAURENTIIS,; M.C. DÍAZ,; M.LASAGA,; D.PISERA,; A. SEILICOVICH; B. DUVILANSKI,
Revista:
European Journal of Endocrinology
Editorial:
SOC. EUROPJ ENDOCRINOL
Referencias:
Año: 2000 vol. 143 p. 279 - 284
ISSN:
0804-4643
Resumen:
Objective: In order to determine the mechanism by which nitric oxide (NO) inhibits prolactin release,
we investigated the participation of cGMP-dependent cAMP-phosphodiesterases (PDEs) and protein
kinase G (PKG) in this effect of NO.
Methods: Anterior pituitary glands of male rats were incubated with inhibitors of PDE and PKG with
or without sodium nitroprusside (NP). Prolactin release, and cAMP and cGMP concentrations were
determined by RIA.
Results and conclusions: The inhibitory effect of NP (0.5 mmol/l) on prolactin release and cAMP
concentration was blocked by EHNA (10±4 mol/l) and HL-725 (10±4 mol/l), inhibitors of cGMPstimulated
cAMP-PDE (PDE2). 8-Br-cGMP (10±4 and 10±3 mol/l), which mimics cGMP as a mediator
of NP effects on prolactin release, also decreased cAMP concentration. Zaprinast (10±4 mol/l), a
selective inhibitor of speci®c cGMP-PDE (PDE5), potentiated the NP effect on cAMP concentration.
Rp-8-[(4-chlorophenyl)thio]-cGMP triethylamine (Rp-8-cGMP, 10±7±10±6 mol/l), an inhibitor of PKG,
reversed the effect of NP on prolactin release. The present study suggests that several mechanisms
are involved in the inhibitory effect of NO on prolactin release. The activation of PDE2 by cGMP
may mediate the inhibitory effect of NO on cAMP concentration and therefore on prolactin release.
NO-activated PKG may also be participating in the inhibitory effect of NO on prolactin release.