Nitric oxide acutely modulates hypothalamic and neurohypophyseal carbon monoxide and hydrogen sulphide production to control vasopressin, oxytocin and atrial natriuretic peptide release in rats

Autor(es)

Coletti, Ricardo ^[1] ; Medeiros de Lima, Juliana Bezerra ^[1] ; Veanholi Vechiato, Fernanda Maria ^{[2, 3]} ; de Oliveira, Fabiana Lucio ^[4] ; Debarba, Lucas Kniess ^[1] ; Almeida-Pereira, Gislaine ^[1] ; Kagohara Elias, Lucila Leico ^[1] ; Antunes-Rodrigues, Jose ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Physiol, Ribeirao Preto - Brazil

^[2] Auxilium Salesian Catholic Univ Ctr UniSALESIANO, Aracatuba - Brazil

^[3] Paulista Univ UNIP, Aracatuba - Brazil

^[4] Fed Inst Educ Sci & Technol Southern Minas Gerais, Muzambinho - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Journal of Neuroendocrinology; v. 31, n. 2 FEB 2019.
• Citações Web of Science: 2

Resumo

Nitric oxide (NO) negatively modulates the secretion of vasopressin (AVP), oxytocin (OT) and atrial natriuretic peptide (ANP) induced by the increase in extracellular osmolality, whereas carbon monoxide (CO) and hydrogen sulphide (H2S) act to potentiate it; however, little information is available for the osmotic challenge model about whether and how such gaseous systems modulate each other. Therefore, using an acute ex vivo model of hypothalamic and neurohypophyseal explants (obtained from male 6/7-week-old Wistar rats) under conditions of extracellular iso- and hypertonicity, we determined the effects of NO (600 mu mol L-1 sodium nitroprusside), CO (100 mu mol L-1 tricarbonylchloro{[}glycinato]ruthenium {[}II]) and H2S (10 mmol L-1 sodium sulphide) donors and nitric oxide synthase (NOS) (300 mu mol L-1 N-omega-methyl-l-arginine {[}LNMMA]), haeme oxygenase (HO) (200 mu mol L-1 Zn(II) deuteroporphyrin IX 2,4-bis-ethylene glycol {[}ZnDPBG]) and cystathionine beta-synthase (CBS) (100 mu mol L-1 aminooxyacetate {[}AOA]) inhibitors on the release of hypothalamic ANP and hypothalamic and neurohypophyseal AVP and OT, as well as on the activities of NOS, HO and CBS. LNMMA reversed hyperosmolality-induced NOS activity, and enhanced hormonal release by the hypothalamus and neurohypophysis, in addition to increasing CBS and hypothalamic HO activity. AOA decreased hypothalamic and neurohypophyseal CBS activity and hormonal release, whereas ZnDPBG inhibited HO activity and hypothalamic hormone release; however, in both cases, AOA did not modulate NOS and HO activity and ZnDPBG did not affect NOS and CBS activity. Thus, our data indicate that, although endogenous CO and H2S positively modulate AVP, OT and ANP release, only NO plays a concomitant role of modulator of hormonal release and CBS activity in the hypothalamus and neurohypophysis and that of HO activity in the hypothalamus during an acute osmotic stimulus, which suggests that NO is a key gaseous controller of the neuroendocrine system. (AU)

• Processo FAPESP: 14/07372-3 - Interação dos sistemas gasosos do H2S, NO e CO na secreção in vitro de vasopressina, ocitocina e peptídeo atrial natriurético pelo hipotálamo médio basal e neuroipófise em resposta à hiperosmolalidade extracelular
• Beneficiário: Ricardo Coletti
• Modalidade de apoio: Bolsas no Brasil - Doutorado