Nitric oxide acutely modulates hypothalamic and neurohypophyseal carbon monoxide and hydrogen sulphide production to control vasopressin, oxytocin and atrial natriuretic peptide release in rats
Nitric oxide acutely modulates hypothalamic and neurohypophyseal carbon monoxide and hydrogen sulphide production to control vasopressin, oxytocin and atrial natriuretic peptide release in rats
复制标题
DOI：
10.1111/jne.12686
复制
发表时间：
2019-02-01
影响因子：
3.2
通讯作者：
Antunes-Rodrigues, Jose
中科院分区：
文献类型：
--
作者：
Coletti, Ricardo;Medeiros de Lima, Juliana Bezerra;Antunes-Rodrigues, Jose
一氧化氮（NO）负性调节加压素（AVP），催产素（OT）和心钠素（ANP）的分泌诱导的细胞外渗透压的增加，而一氧化碳（CO）和硫化氢（H2S）的行为，以加强它，然而，很少有信息可用于渗透压挑战模型是否以及如何这样的气体系统相互调节。因此，使用下丘脑和神经垂体外植体的急性离体模型，（从雄性6/7周龄Wistar大鼠获得）在细胞外等渗和高渗的条件下，我们确定了NO的影响，（600 μ mol L-1硝普钠），CO（100 μ mol L-1三羰基氯[甘氨酸]钌[II]）和H2S（10 mmol L-1硫化钠）供体和一氧化氮合酶（NOS）（300 μ mol L-1 N-ω-甲基-l-精氨酸[LNMMA]），血红素加氧酶（HO）（200 μ mol L-1 Zn（II）次卟啉IX 2，4-双乙二醇[ZnDPBG]）和胱硫醚β-合酶（CBS）（100 μ mol L-1氨氧基乙酸[AOA]）抑制下丘脑ANP和下丘脑及神经垂体AVP和OT的释放，以及NOS的活性，HO和CBS。LNMMA逆转高渗诱导的NOS活性，并增强下丘脑和神经垂体的激素释放，除了增加CBS和下丘脑HO活性。AOA降低下丘脑和神经垂体CBS活性和激素释放，而ZnDPBG抑制HO活性和下丘脑激素释放;然而，在这两种情况下，AOA没有调节NOS和HO活性和ZnDPBG没有影响NOS和CBS活性。因此，我们的数据表明，虽然内源性CO和H2S正调节AVP，OT和ANP的释放，只有NO起着伴随的作用，下丘脑和神经垂体的激素释放和CBS活性的调制器和HO活性在下丘脑在急性渗透刺激，这表明NO是一个关键的气体控制器的神经内分泌系统。
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.