Bioscience Reports (2010) 30, 351-357 - D. A. Gomes and others

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Bioscience Reports (2010) 30, (351–357) (Printed in Great Britain)

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Original Paper

Carbon monoxide and nitric oxide modulate hyperosmolality-induced oxytocin secretion by the hypothalamus in vitro

Dayane Aparecida Gomes*, Alexandre Giusti‑Paiva†, Renato Rizo Ventura*, Lucila Leico Kagohara Elias*, Fernando Queiroz Cunha* and Jose Antunes‑Rodrigues*¹

*Universidade de Sao Paulo, Ribeirao Preto, SP, Brazil, and †Universidade Federal de Alfenas, Alfenas, MG, Brazil

Key words: carbon monoxide, haem oxygenase, hypothalamus, nitric oxide, osmotic regulation, oxytocin (OT).

Abbreviations used: ANP, atrial natriuretic peptide; AVP, vasopressin; AV3V, anteroventral third ventricle; CNS, central nervous system; HO, haem oxygenase; KRBG, Krebs–Ringer bicarbonate buffer; LDH, lactate dehydrogenase; L-NAME, N^G-nitro-L-arginine methyl ester; L-NMMA: N^G-monomethyl-L-arginine; MnPO, median preoptic nucleus; NOS, nitric oxide synthase; ODQ, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; OT, oxytocin; OVLT, organum vasculosum of the lamina terminalis; PVN, paraventricular nucleus; SFO, subfornical organ; sGC, soluble guanylate cyclase; SIN-1, 3-morpholinosydnonimine hydrochloride; SNAP, S-nitroso-N-acetyl-DL-penicillamine; SNP, sodium nitroprusside; SON, supraoptic nucleus; ZnPPIX, protoporphyrin IX zinc(II).

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.