Effects of hydrogen sulfide (H2S) on water intake and vasopressin and oxytocin secretion induced by fluid deprivation

Coletti, Ricardo; Almeida-Pereira, Gislaine; Elias, Lucila Leico Kagohara; Antunes‐Rodrigues, José

doi:10.1016/j.yhbeh.2014.11.008

Cited by 30 publications

(46 citation statements)

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“…Ferric hHO‐1‐haeme was shown to form a stable 6‐coordinated complex with NO that inhibits HO activity and NO binds tightly to CBS ferrous haeme and weakly to the ferric haeme, decreasing sulphide formation in both cases. Such data from the literature support our findings, being indicative of interactions capable of negatively modulating hormonal release and NOS activity itself, in addition to CBS and hypothalamic HO activity, for which the products CO and H 2 S are considered to be stimulatory to hormone release during osmotic challenge …”

Section: Discussionsupporting

confidence: 89%

“…l ‐cysteine is the substrate of CBS, which yields H 2 S in the presence (or not) of homocysteine, mandatorily demanding pyridoxal‐5′‐phosphate; l ‐cysteine is also the substrate of cysteine aminotransferase, an enzyme that produces 3‐mercaptopyruvate, which, in turn, is a substrate of 3MST . Regardless of the generation pathway, H 2 S has been shown to act on depolarising magnocellular neurones in a dose‐dependent fashion, increasing plasma AVP and OT concentrations, and decreasing the hypothalamic nitrate content of 24‐hour water‐deprived rats …”

Section: Introductionmentioning

confidence: 99%

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

Coletti

Lima

Vechiato

et al. 2019

J Neuroendocrinology

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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 (H 2 S) 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 μmol L -1 sodium nitroprusside), CO (100 μmol L -1 tricarbonylchloro[glycinato]ruthenium [II]) and H 2 S (10 mmol L -1 sodium sulphide) donors and nitric oxide synthase (NOS) (300 μmol L -1 N ω -methyl-l-arginine [LNMMA]), haeme oxygenase (HO) (200 μmol L -1 Zn(II) deuteroporphyrin IX 2,4-bisethylene glycol [ZnDPBG]) and cystathionine β-synthase (CBS) (100 μmol 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 H 2 S 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. K E Y W O R D S atrial natriuretic peptide, carbon monoxide, hydrogen sulphide, nitric oxide, oxytocin, vasopressin 2 of 16 | COLETTI ET aL. | INTRODUC TI ONThe release of vasopressin (AVP) and oxytocin (OT) by the hypothalamus and the neurohypophysis is a very complex and robust process that is controlled by many factors produced both within and outside these brain sites. 1 Among such factors, atrial natriuretic peptide (ANP) stands out as established modulator of thirst and AVP release, 2-4 whereas a novel class of small polar molecules, mainly represented by nitric oxide (NO), carbon monoxide (CO) and hydrogen sulphide (H 2 S), 5 have achieved prominence more recently.NO is produced from the amino acid l-arginine via a reaction catalysed by the enzyme nitric oxide synthase (NOS), which presents three major isoforms (neuronal [nNOS], endothelial [eNOS] and inducible [iNOS]), where, in the central nervous system (CNS), nNOS is considered the main isoform. 6 NOS active form is usually dimeric and exhibits an oxygenase domain, in which, in addition to ...

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

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

Coletti

Lima

Vechiato

et al. 2019

J Neuroendocrinology

View full text Add to dashboard Cite

show abstract

“…Regarding hydromineral balance, Khademullah and Ferguson (56) recently showed through electrophysiological approaches that exogenous H 2 S increases the excitability of PVN MNs, which most likely produce direct effects on AVP and OT secretion. In addition, a recent report of our group demonstrated that water deprivation increases the hypothalamic activity of H 2 S-generating enzymes and that the icv administration of an H 2 S donor potentiates neurohypophyseal hormone secretion, as well as decreases hypothalamic nitrite/nitrate contents in water-deprived rats, indicating a reduced NO production (24). Although there are very few reports in the literature devoted to the investigation of H 2 S action in hypothalamic neurotransmission, a possible site-specific and complex interaction between NO, CO, and H 2 S and their specific enzymatic/ intracellular machineries will likely appear in the near future as a promising field of investigation.…”

Section: Figure 3 Overview Of Nitric Oxide (No) Effects On Magnocellmentioning

confidence: 80%

Gaseous Modulators in the Control of the Hypothalamic Neurohypophyseal System

et al. 2015

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Nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S) are gaseous molecules produced by the brain. Within the hypothalamus, gaseous molecules have been highlighted as autocrine and paracrine factors regulating endocrine function. Therefore, in the present review, we briefly discuss the main findings linking NO, CO, and H2S to the control of body fluid homeostasis at the hypothalamic level, with particular emphasis on the regulation of neurohypophyseal system output.

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“…Several studies have demonstrated that peripheral osmoreceptors modulated AVP release from the posteriorpituitary into the circulation, and these osmoreceptors are located within the liver and portal vein region. Another possible explanation is that hepatic IR may induce the release of gastrointestinal hormones or ouabain-like substances, which activate the hypothalamic nuclei leading to AVP secretion [18, 19]. The detailed mechanism needs to be investigated in future studies.…”

Section: Discussionmentioning

confidence: 99%

Signaling through hepatocyte vasopressin receptor 1 protects mouse liver from ischemia-reperfusion injury

et al. 2016

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Terlipressin has been used extensively in the management of certain complications associated with end-stage liver diseases (ESLDs). In our pilot study, terlipressin treatment showed beneficial effects on liver function in patients with decompensated cirrhosis, however whether it plays a role in liver ischemia-reperfusion injury (IRI) remains unknown. Using a mouse nonlethal hepatic IR model, we found terlipressin administration significantly ameliorated IR-induced liver apoptosis, necrosis and inflammation. Furthermore, despite its known effect on visceral vasoconstriction, hemodynamic evaluation of murine hepatic tissue after IR revealed no change of overall hepatic blood flow after terlipressin treatment. Further studies identified the upregulation of vasopressin receptor 1 (V1R) expression on hepatocytes upon IR. In isolated hepatocyte hypoxia/reoxygenation model, the active component of terlipressin, lysine vasopressin, conferred hepatocytes resistant to oxidative stress-induced apoptosis. Mechanistic studies revealed the V1R engagement activated the Wnt/β-catenin/FoxO3a/AKT pathway, which subsequently circumvented the proapoptotic events, thus ameliorated hepatocyte apoptosis. Furthermore, genetic knockdown of V1R expression in hepatocyte cell lines or blockade of this signaling pathway abrogated such protective effect. Conclusion: These data highlight the functional importance of the hepatocyte V1R/Wnt/β-catenin/FoxO3a/AKT pathway in protecting liver from oxidative stress-induced injury.

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Effects of hydrogen sulfide (H2S) on water intake and vasopressin and oxytocin secretion induced by fluid deprivation

Cited by 30 publications

References 50 publications

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

Gaseous Modulators in the Control of the Hypothalamic Neurohypophyseal System

Signaling through hepatocyte vasopressin receptor 1 protects mouse liver from ischemia-reperfusion injury

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