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Carbon monoxide and nitric oxide modulate hyperosmolality‐induced oxytocin secretion by hypothalamus explant
Author(s) -
Gomes Dayane Aparecida,
Sladek Celia D,
Elias Lucila Leico Kagohara,
AntunesRodrigues Jose
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a507-d
Subject(s) - nitric oxide , chemistry , sodium nitroprusside , oxytocin , endocrinology , medicine , stimulation , nitric oxide synthase , heme oxygenase , soluble guanylyl cyclase , heme , biochemistry , enzyme , biology , cyclic gmp , organic chemistry
We evaluated the participation of the nitric oxide (NO) and carbon monoxide (CO) in the oxytocin (OT) release induced by osmotic stimulation of hypothalamus fragments in vitro. The increase in the medium osmolality induced a significant increase in OT release which was associated with a decrease in the nitric oxide synthase activity and nitrate production. The NO donors: sodium nitroprusside, S‐nitroso‐N‐acetylpenicillamine and 3‐morpholinylsydnoneimine chloride promoted a significant decrease in the OT release in response to hyperosmolality. This response is mediated by the activation of guanylyl cyclase (GC) and cGMP generation. GC inhibition blocked the response induced by SNP. 8‐Bromoguanosine‐cGMP (8‐Bromo cGMPc), a cell‐permeable cGMP analog, inhibits OT release mimicking the results obtained with NO donors. In addition, heme‐oxigenase (HO) stimulation with heme‐L‐lysinate caused a significant increase in OT release. In contrast, HO inhibition with Zinc deuteroporphyrin 2,4‐bis glycol (ZnDPBG) decreases the OT release and increases NOS activity. The inhibition of hormonal secretion was blocked by GC inhibitor suggesting that the inhibitory action of the ZnDPBG is in part mediated by activation of the GC‐GMPc system. In conclusion, these results suggest a important role of the NO/CO systems in modulation of OT secretion from BH fragments.