Endogenous Nitric Oxide Inhibits Growth Hormone Secretion through Cyclic Guanosine Monophosphate-Dependent Mechanisms in GH3 Cells

Constitutive nitric oxide synthase (NOS) is expressed in rat adenohypophysis and clonal GH3 cells. The mechanisms of action of nitric oxide (NO) to inhibit hormone secretion and the possible role of (6R)-5, 6, 7, 8-tetrahydro-L-biopterin (THB) in the action of endogenous NO were studied in GH3 cells...

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Published in:ENDOCRINE JOURNAL 1999, Vol.46(6), pp.779-785
Main Authors: TSUMORI, MICHIHIRO, MURAKAMI, YOSHIO, KOSHIMURA, KUNIO, KATO, YUZURU
Format: Article
Language:English
Subjects:
Animals
Biopterins - analogs & derivatives
Biopterins - physiology
Cell Line
Cyclic GMP
Cyclic GMP - analogs & derivatives
Cyclic GMP - antagonists & inhibitors
Cyclic GMP - pharmacology
Cyclic GMP - physiology
Dose-Response Relationship, Drug
Drug Synergism
Enzyme Inhibitors - pharmacology
GH3 cells
Growth Hormone - metabolism
Nitric oxide
Nitric Oxide - physiology
Oxyhemoglobins - pharmacology
Rats
Tetrahydrobiopterin
Thionucleotides - pharmacology
Thyrotropin-Releasing Hormone - pharmacology
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Summary:Constitutive nitric oxide synthase (NOS) is expressed in rat adenohypophysis and clonal GH3 cells. The mechanisms of action of nitric oxide (NO) to inhibit hormone secretion and the possible role of (6R)-5, 6, 7, 8-tetrahydro-L-biopterin (THB) in the action of endogenous NO were studied in GH3 cells. Inhibiting NOS with NG-nitro-L-arginine or trapping NO with oxyhemoglobin enhanced both the basal and TRH-stimulated rat GH release. Sodium nitroprusside did not further decrease either the basal or the TRH-stimulated GH secretion, suggesting that endogenous NO exerted the maximal inhibitory effect. Inhibition of de novo synthesis of THB increased GH secretion. A cyclic guanosine-monophosphate (cGMP) antagonist did not increase the basal GH secretion but enhanced TRH-induced GH release. These findings suggest that endogenous NO plays an inhibitory role on basal GH release and TRH-stimulated hormone release from GH3 cells in an autocrine or paracrine fashion, at least partly, through a cGMP-dependent pathway. It is also suggested that endogenous THB plays a role in NO production and subsequent inhibition of hormone secretion in GH3 cells.
ISSN:0918-8959
1348-4540
DOI:10.1507/endocrj.46.779