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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.
J Neuroendocrinol. 2019 02; 31(2):e12686.JN

Abstract

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 (H2 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 H2 S (10 mmol L-1 sodium sulphide) donors and nitric oxide synthase (NOS) (300 μmol L-1 Nω -methyl-l-arginine [LNMMA]), haeme oxygenase (HO) (200 μmol L-1 Zn(II) deuteroporphyrin IX 2,4-bis-ethylene 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 H2 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.

Authors+Show Affiliations

Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.Auxilium Salesian Catholic University Center - UniSALESIANO, Araçatuba, Brazil. Paulista University - UNIP, Araçatuba, Brazil.Federal Institute of Education, Science and Technology of Southern Minas Gerais, Muzambinho, Brazil.Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30633838

Citation

Coletti, Ricardo, et al. "Nitric Oxide Acutely Modulates Hypothalamic and Neurohypophyseal Carbon Monoxide and Hydrogen Sulphide Production to Control Vasopressin, Oxytocin and Atrial Natriuretic Peptide Release in Rats." Journal of Neuroendocrinology, vol. 31, no. 2, 2019, pp. e12686.
Coletti R, de Lima JBM, Vechiato FMV, et al. Nitric oxide acutely modulates hypothalamic and neurohypophyseal carbon monoxide and hydrogen sulphide production to control vasopressin, oxytocin and atrial natriuretic peptide release in rats. J Neuroendocrinol. 2019;31(2):e12686.
Coletti, R., de Lima, J. B. M., Vechiato, F. M. V., de Oliveira, F. L., Debarba, L. K., Almeida-Pereira, G., Elias, L. L. K., & Antunes-Rodrigues, J. (2019). Nitric oxide acutely modulates hypothalamic and neurohypophyseal carbon monoxide and hydrogen sulphide production to control vasopressin, oxytocin and atrial natriuretic peptide release in rats. Journal of Neuroendocrinology, 31(2), e12686. https://doi.org/10.1111/jne.12686
Coletti R, et al. Nitric Oxide Acutely Modulates Hypothalamic and Neurohypophyseal Carbon Monoxide and Hydrogen Sulphide Production to Control Vasopressin, Oxytocin and Atrial Natriuretic Peptide Release in Rats. J Neuroendocrinol. 2019;31(2):e12686. PubMed PMID: 30633838.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitric oxide acutely modulates hypothalamic and neurohypophyseal carbon monoxide and hydrogen sulphide production to control vasopressin, oxytocin and atrial natriuretic peptide release in rats. AU - Coletti,Ricardo, AU - de Lima,Juliana Bezerra Medeiros, AU - Vechiato,Fernanda Maria Veanholi, AU - de Oliveira,Fabiana Lucio, AU - Debarba,Lucas Kniess, AU - Almeida-Pereira,Gislaine, AU - Elias,Lucila Leico Kagohara, AU - Antunes-Rodrigues,José, Y1 - 2019/02/12/ PY - 2018/07/16/received PY - 2019/01/07/revised PY - 2019/01/07/accepted PY - 2019/1/12/pubmed PY - 2020/8/18/medline PY - 2019/1/12/entrez KW - atrial natriuretic peptide KW - carbon monoxide KW - hydrogen sulphide KW - nitric oxide KW - oxytocin KW - vasopressin SP - e12686 EP - e12686 JF - Journal of neuroendocrinology JO - J Neuroendocrinol VL - 31 IS - 2 N2 - 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 (H2 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 H2 S (10 mmol L-1 sodium sulphide) donors and nitric oxide synthase (NOS) (300 μmol L-1 Nω -methyl-l-arginine [LNMMA]), haeme oxygenase (HO) (200 μmol L-1 Zn(II) deuteroporphyrin IX 2,4-bis-ethylene 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 H2 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. SN - 1365-2826 UR - https://www.unboundmedicine.com/medline/citation/30633838/Nitric_oxide_acutely_modulates_hypothalamic_and_neurohypophyseal_carbon_monoxide_and_hydrogen_sulphide_production_to_control_vasopressin_oxytocin_and_atrial_natriuretic_peptide_release_in_rats_ L2 - https://doi.org/10.1111/jne.12686 DB - PRIME DP - Unbound Medicine ER -