Supplementation with the symbiotic formulation Prodefen® increases neuronal nitric oxide synthase and decreases oxidative stress in superior mesenteric artery from spontaneously hypertensive rats
Entity
UAM. Departamento de Farmacología; UAM. Departamento de FisiologíaPublisher
Multidisciplinary Digital Publishing InstituteDate
2022-03-30Citation
10.3390/antiox11040680
Antioxidants 11.4 (2022): 680
ISSN
2076-3921(online)DOI
10.3390/antiox11040680Funded by
This research was funded by CiberCV (Grant number: CB16/11/00286), the Ministerio de Ciencia e Innovación (PID2020-116498RB-I00, and CDTI -Center for Industrial Technological Development-project PID 2020-FEDER Funds), and R+D projects for young researchers, Universidad Autónoma de Madrid-Comunidad de Madrid (SI1-PJI-2019-00321)Project
Gobierno de España. PID2020-116498RB-I00; Gobierno de España. PID 2020-FEDER Funds; Comunidad de Madrid. SI1-PJI-2019-00321Editor's Version
https://doi.org/10.3390/antiox11040680Subjects
hypertension; neuronal nitric oxide; Nrf2; oxidative stress; perivascular mesenteric innervation; PI3K-AKT; protein kinase A; protein kinase C; synbiotic; MedicinaRights
© 2022 by the authorsAbstract
In recent years, gut dysbiosis has been related to some peripheral vascular alterations linked to hypertension. In this work, we explore whether gut dysbiosis is related to vascular innervation dysfunction and altered nitric oxide (NO) production in the superior mesenteric artery, one of the main vascular beds involved in peripheral vascular resistance. For this purpose, we used spontaneously hypertensive rats, either treated or not with the commercial synbiotic formulation Prodefen® (108 colony forming units/day, 4 weeks). Prodefen® diminished systolic blood pressure and serum endotoxin, as well as the vasoconstriction elicited by electrical field stimulation (EFS), and enhanced acetic and butyric acid in fecal samples, and the vasodilation induced by the exogenous NO donor DEA-NO. Unspecific nitric oxide synthase (NOS) inhibitor L-NAME increased EFS-induced vasoconstriction more markedly in rats supplemented with Prodefen®. Both neuronal NO release and neuronal NOS activity were enhanced by Prodefen®, through a hyperactivation of protein kinase (PK)A, PKC and phosphatidylinositol 3 kinase-AKT signaling pathways. The superoxide anion scavenger tempol increased both NO release and DEA-NO vasodilation only in control animals. Prodefen® caused an increase in both nuclear erythroid related factor 2 and superoxide dismutase activities, consequently reducing both superoxide anion and peroxynitrite releases. In summary, Prodefen® could be an interesting non-pharmacological approach to ameliorate hypertension
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Google Scholar:Méndez-Albiñana, Pablo
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Martínez-González, Ángel
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Camacho-Rodríguez, Laura
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Ferreira Lazarte, Alvaro
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Villamiel, Mar
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Rodrigues Díez, Raquel
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Balfagón, Gloria
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García Redondo, Ana Belén
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Prieto Nieto, María Isabel
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Blanco Rivero, Javier
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