Carbon monoxide and nitric oxide modulate hyperosmolality-induced oxytocin secretion by the hypothalamus in vitro.
OT (oxytocin) is secreted from the posterior pituitary gland, and its secretion has been shown to be modulated by NO (nitric oxide). In rats, OT secretion is also stimulated by hyperosmolarity of the extracellular fluid. Furthermore, NOS (nitric oxide synthase) is located in hypothalamic areas involved in fluid balance control. In the present study, we evaluated the role of the NOS/NO and HO (haem oxygenase)/CO (carbon monoxide) systems in the osmotic regulation of OT release from rat hypothalamus in vitro. We conducted experiments on hypothalamic fragments to determine the following: (i) whether NO donors and NOS inhibitors modulate OT release and (ii) whether the changes in OT response occur concurrently with changes in NOS or HO activity in the hypothalamus. Hyperosmotic stimulation induced a significant increase in OT release that was associated with a reduction in nitrite production. Osmotic stimulation of OT release was inhibited by NO donors. NOS inhibitors did not affect either basal or osmotically stimulated OT release. Blockade of HO inhibited both basal and osmotically stimulated OT release, and induced a marked increase in NOS activity. These results indicate the involvement of CO in the regulation of NOS activity. The present data demonstrate that hypothalamic OT release induced by osmotic stimuli is modulated, at least in part, by interactions between NO and CO.
Gomes
Dayane Aparecida
DA
Universidade de Sao Paulo, Ribeirao Preto, SP, Brazil.
Giusti-Paiva
Alexandre
A
Ventura
Renato Rizo
RR
Elias
Lucila Leico Kagohara
LL
Cunha
Fernando Queiroz
FQ
Antunes-Rodrigues
Jose
J
D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000378:metabolism; D000818:Animals; D002248:Carbon Monoxide / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D009599:Nitroprusside / Q000378:metabolism; D009997:Osmotic Pressure; D010069:Oxadiazoles / Q000378:metabolism; D010121:Oxytocin / Q000378:metabolism*; D011810:Quinoxalines / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
C095284:1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one; D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D009573:Nitrites; D010069:Oxadiazoles; D011810:Quinoxalines; D009599:Nitroprusside; D015124:8-Bromo Cyclic Adenosine Monophosphate; D009569:Nitric Oxide; D010121:Oxytocin; D002248:Carbon Monoxide; D019001:Nitric Oxide Synthase