Angiotensin-II-induced reactive oxygen species along the SFO-PVN-RVLM pathway: implications in neurogenic hypertension

Braga, Valdir A.; Medeiros, Isac A.; Ribeiro, Thais Porto; França-Silva, Maria S.; Botelho-Ono, Mayumi S.; Guimarães, Drielle D.

doi:10.1590/s0100-879x2011007500088

Cited by 84 publications

(71 citation statements)

References 54 publications

(68 reference statements)

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“…These data suggest the involvement of the NO-sGC-cGMP pathway in the relaxant response induced by Oxime S1. In a similar way, Chalupský et al and Veras et al [13,14] demonstrated that the effects of several non-aromatic substituted oximes derivatives involve the NO-sGC-cGMP pathway.…”

Section: Oxime S1 Produces Vasorelaxation Via Activation Of the No-sgmentioning

confidence: 79%

“…Previous studies aiming to evaluate the vascular effects induced by oximes were performed in arteries without endothelium suggesting the involvement of the NO-cGMP pathway [13,14]. The aim of the present study was to investigate the cardiovascular effects produced by a new synthetized oxime, the 3-hydroxy-4-(hydroxyimino)-2-(3-methylbut-2-enylnaphtalen-1(4H)-one (Oxime S1, Figure 1), which is a semi-natural naphthoquinone derivative of lapachol extracted from Tabebuia avallanedae Lor.Ex.Gris (Bignoniaceae), which formula is shown bellow.…”

Section: Introductionmentioning

confidence: 99%

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Vasorelaxation Induced by a New Naphthoquinone-Oxime is Mediated by NO-sGC-cGMP Pathway

et al. 2014

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It has been established that oximes cause endothelium-independent relaxation in blood vessels. In the present study, the cardiovascular effects of the new oxime 3-hydroxy-4-(hydroxyimino)-2-(3-methylbut-2-enylnaphtalen-1(4H)-one (Oxime S1) derived from lapachol were evaluated. In normotensive rats, administration of Oxime S1 (10,15, 20 and 30 mg/Kg, i.v.) produced dose-dependent reduction in blood pressure. In isolated aorta and superior mesenteric artery rings, Oxime S1 induced endothelium-independent and concentration-dependent relaxations (10 −8 M to 10 −4 M). In addition, Oxime S1-induced vasorelaxations were attenuated by hydroxocobalamin or methylene blue in aorta and by PTIO or ODQ in mesenteric artery rings, suggesting a role for the nitric oxide (NO) pathway. Additionally, Oxime S1 (30 and 100 µM) significantly increased NO concentrations (13.9 ± 1.6 nM and 17.9 ± 4.1 nM, respectively) measured by nitric oxide microsensors. Furthermore, pre-contraction with KCl (80 mM) prevented Oxime S1-derived vasorelaxation in endothelium-denuded aortic rings. Of note, combined treatment with potassium channel inhibitors also reduced Oxime S1-mediated vasorelaxation suggesting OPEN ACCESSMolecules 2014, 19 9774 a role for potassium channels, more precisely K ir , K v and K ATP channels. We observed the involvement of BK Ca channels in Oxime S1-induced relaxation in mesenteric artery rings.In conclusion, these data suggest that the Oxime S1 induces hypotension and vasorelaxation via NO pathway by activating soluble guanylate cyclase (sGC) and K + channels.

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Section: Oxime S1 Produces Vasorelaxation Via Activation Of the No-sgmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Vasorelaxation Induced by a New Naphthoquinone-Oxime is Mediated by NO-sGC-cGMP Pathway

et al. 2014

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“…3A). Such decrease is associated with an increase of NADPH oxidase activity and generation of ROS Braga et al 2011). Coconut oil combined with exercise training improved baroreflex sensitivity in hypertensive rats.…”

Section: Discussionmentioning

confidence: 95%

“…Several studies have shown that there a strong association between hypertension and the formation of reactive oxygen species (ROS) Braga et al 2011;Mei et al 2014). The generation of ROS is involved in cardiovascular autonomic dysfunction and reduction in baroreflex sensitivity Guimarães et al 2012;Nishi et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Coconut oil supplementation and physical exercise improves baroreflex sensitivity and oxidative stress in hypertensive rats

Alves

Porpino

Monteiro

et al. 2015

Appl. Physiol. Nutr. Metab.

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Abstract:The hypothesis that oral supplementation with virgin coconut oil (Cocos nucifera L.) and exercise training would improve impaired baroreflex sensitivity (BRS) and reduce oxidative stress in spontaneously hypertensive rats (SHR) was tested. Adult male SHR and Wistar Kyoto rats (WKY) were divided into 5 groups: WKY + saline (n = 8); SHR + saline (n = 8); SHR + coconut oil (2 mL·day −1 , n = 8); SHR + trained (n = 8); and SHR + trained + coconut oil (n = 8). Mean arterial pressure (MAP) was recorded and BRS was tested using phenylephrine (8 g/kg, intravenous) and sodium nitroprusside (25 g·kg −1 , intravenous). Oxidative stress was measured using dihydroethidium in heart and aorta. SHR + saline, SHR + coconut oil, and SHR + trained group showed higher MAP compared with WKY + saline (175 ± 6, 148 ± 6, 147 ± 7 vs. 113 ± 2 mm Hg; p < 0.05). SHR + coconut oil, SHR + trained group, and SHR + trained + coconut oil groups presented lower MAP compared with SHR + saline group (148 ± 6, 147 ± 7, 134 ± 8 vs. 175 ± 6 mm Hg; p < 0.05). Coconut oil combined with exercise training improved BRS in SHR compared with SHR + saline group (−2.47 ± 0.3 vs. −1.39 ± 0.09 beats·min −1 ·mm Hg −1 ; p < 0.05). SHR + saline group showed higher superoxide levels when compared with WKY + saline (774 ± 31 vs. 634 ± 19 arbitrary units (AU), respectively; p < 0.05). SHR + trained + coconut oil group presented reduced oxidative stress compared with SHR + saline in heart (622 ± 16 vs. 774 ± 31 AU, p < 0.05). In aorta, coconut oil reduced oxidative stress in SHR compared with SHR + saline group (454 ± 33 vs. 689 ± 29 AU, p < 0.05). Oral supplementation with coconut oil combined with exercise training improved impaired BRS and reduced oxidative stress in SHR.Key words: virgin coconut oil, swimming, hypertension, baroreflex, antioxidant. Résumé :On vérifie l'hypothèse selon laquelle la supplémentation per os en huile de coco (Cocos nucifera L.) vierge et l'entraînement physique atténuent le dérèglement de la sensibilité du baroréflexe (« BRS ») et diminuent le stress oxydatif chez des rats spontanément hypertendus (« SHR »). On répartit des rats mâles adultes SHR et Wistar Kyoto (« WKY ») en cinq groupes : WKY + saline (n = 8); SHR + saline (n = 8); SHR + huile de coco (2 mL·jour −1 , n = 8); SHR + entraînés (n = 8) et SHR + entraînés + huile de coco (n = 8). On enregistre la pression artérielle moyenne (« MAP ») et on évalue la BRS par l'administration de phényléphrine (8 g·kg −1 , intraveineux) et de nitroprussiate de sodium (25 g·kg −1 , intraveineux). On évalue le stress oxydatif par l'administration de dihydroéthidium dans le coeur et l'aorte. Les groupes SHR + saline, SHR + huile de coco et SHR + entraînés présentent une MAP plus élevée comparativement au groupe WKY + saline (175 ± 6, 148 ± 6, 147 ± 7 vs 113 ± 2 mm Hg, p < 0,05). Les groupes SHR + huile de coco, SHR + entraînés, SHR + entraînés + huile de coco présentent une MAP plus basse comparativement au groupe SHR + saline (148 ± 6, 147 ± 7, 134 ± 8 vs 175 ± 6 mm Hg, p < 0,05). L'hui...

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“…Critical to this regulation is the peptide angiotensin II (ANG II), which can elicit increases in sympathetic outflow and blood pressure in normotensive rats by acting via its type 1 receptors (AT 1 R) in the PVN (9,11,36). Further, in animal models of neurogenic hypertension such as the spontaneously hypertensive rat, it is clear that overactivity of ANG II/AT 1 R in the PVN makes a significant contribution to the raised blood pressure seen in these animals (2,10,16,18). Until recently, investigations focused on the direct neuronal actions of ANG II via AT 1 R in the PVN and whether these effects are enhanced in hypertension (5,6,23).…”

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confidence: 99%

Interleukin-10 inhibits angiotensin II-induced decrease in neuronal potassium current

Jiang

Shi

Desland

et al. 2013

American Journal of Physiology-Cell Physiology

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Jiang N, Shi P, Desland F, Kitchen-Pareja MC, Sumners C. Interleukin-10 inhibits angiotensin II-induced decrease in neuronal potassium current. Am J Physiol Cell Physiol 304: C801-C807, 2013. First published February 20, 2013 doi:10.1152/ajpcell.00398.2012.-Previously we demonstrated that viral-mediated increased expression of the anti-inflammatory cytokine interleukin-10 within the paraventricular nucleus of the hypothalamus significantly reduces blood pressure in normal rats made hypertensive by infusion of angiotensin II. However, the exact cellular locus of this interleukin-10 action within the paraventricular nucleus is unknown. In the present study we tested whether interleukin-10 exerts direct effects at its receptors located on hypothalamic neurons to offset the neuronal excitatory actions of angiotensin II via its type 1 receptors. The results indicated the presence of immunoreactive interleukin-10 receptors on neurons in normal rat paraventricular nucleus and that receptors for this cytokine were also expressed in neurons cultured from the hypothalamus. Patch-clamp electrophysiological recordings from these cultures revealed that extracellular application of interleukin-10 alone did not exert any alterations in neuronal membrane delayed rectifier or transient potassium currents. However, angiotensin II elicited a significant decrease in delayed rectifier potassium current, an effect that was abolished by interleukin-10 application. Since decreases in delayed rectifier potassium current contribute to increased neuronal excitability, this result is consistent with a direct inhibitory action of interleukin-10 on angiotensin-induced excitation of hypothalamic neurons. As such, these data are the first indication of a neuronal locus of action of interleukin-10 to temper the actions of angiotensin II in the hypothalamus. angiotensin II; neuron; interleukin-10; cytokine; potassium current IT IS WELL KNOWN THAT THE central nervous system (CNS) has an important role in the regulation of arterial blood pressure (14,17). This regulation involves interplay between neural circuits that include connections among hypothalamic [paraventricular nucleus (PVN)], brain stem (rostral ventrolateral medulla), and spinal cord (intermediolateral column) sites to ultimately modulate sympathetic outflow and blood pressure (7,17,21). Critical to this regulation is the peptide angiotensin II (ANG II), which can elicit increases in sympathetic outflow and blood pressure in normotensive rats by acting via its type 1 receptors (AT 1 R) in the PVN (9,11,36). Further, in animal models of neurogenic hypertension such as the spontaneously hypertensive rat, it is clear that overactivity of ANG II/AT 1 R in the PVN makes a significant contribution to the raised blood pressure seen in these animals (2,10,16,18). Until recently, investigations focused on the direct neuronal actions of ANG II via AT 1 R in the PVN and whether these effects are enhanced in hypertension (5,6,23). However, studies from our group and others indicate that there i...

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Angiotensin-II-induced reactive oxygen species along the SFO-PVN-RVLM pathway: implications in neurogenic hypertension

Cited by 84 publications

References 54 publications

Vasorelaxation Induced by a New Naphthoquinone-Oxime is Mediated by NO-sGC-cGMP Pathway

Vasorelaxation Induced by a New Naphthoquinone-Oxime is Mediated by NO-sGC-cGMP Pathway

Coconut oil supplementation and physical exercise improves baroreflex sensitivity and oxidative stress in hypertensive rats

Interleukin-10 inhibits angiotensin II-induced decrease in neuronal potassium current

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