Aerobic exercise training increases neuronal nitric oxide release and bioavailability and decreases noradrenaline release in mesenteric artery from spontaneously hypertensive rats

Blanco-Rivero, Javier; Roque, Fernanda Roberta; Sastre, Esther; Caracuel, Laura; Couto, Gisele Kruger; Avendaño, María Soledad; Paula, Suliana Mesquita; Rossoni, Luciana Venturini; Salaíces, Mercedes; Balfagón, Gloria

doi:10.1097/hjh.0b013e32835f749c

Cited by 30 publications

(34 citation statements)

References 48 publications

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“…Several studies have reported that plasma levels of NO Å metabolites, nitrite and nitrosothiols increase during exercise in both rodents and humans (Blanco-Rivero et al, 2013;Calvert, 2011;Kimura et al, 2003;Linke et al, 2008). More recently, Calvert and co-workers showed that sustained cardioprotective effects of 4 weeks of voluntary exercise are mediated by increased phosphorylation of cardiac eNOS ser1177 , leading to an increase in NO Å generation and storage of NO Å metabolites (i.e.…”

Section: Ischemia-reperfusion Injurymentioning

confidence: 96%

“…Of interest, a single bout of either aerobic or resistance exercise increases endothelial-dependent relaxation through NO Å pathways (Faria Tde et al, 2010;Yang et al, 2010). Moreover, improved NOS activity and diminished ROS production have been associated with better vascular function in hypertensive rats submitted to either moderate-or high-intensity aerobic exercise training (Blanco-Rivero et al, 2013;Kimura et al, 2010;Roque et al, 2013a,b;Yang et al, 2011). The use of either ROS scavenger or NOS inhibitor abolishes the improvement of endothelial function mediated by exercise training in coronary arterioles from pigs (Xie et al, 2012).…”

Section: Hypertensionmentioning

confidence: 97%

“…Over the last decades, exercise training has been widely recognized as an important non-pharmacological strategy for the prevention and treatment of hypertension (Blanco-Rivero et al, 2013;Pescatello et al, 2004;Roque et al, 2013b). Exercise decreases blood pressure due to a better aortic baroreceptor gain sensitivity and reduced vascular resistance (Brum et al, 2000;Cornelissen and Fagard, 2005).…”

Section: Hypertensionmentioning

confidence: 99%

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Impact of exercise training on redox signaling in cardiovascular diseases

Campos

Gomes

Ferreira

2013

Food and Chemical Toxicology

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Section: Ischemia-reperfusion Injurymentioning

confidence: 96%

Section: Hypertensionmentioning

confidence: 97%

Section: Hypertensionmentioning

confidence: 99%

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Impact of exercise training on redox signaling in cardiovascular diseases

Campos

Gomes

Ferreira

2013

Food and Chemical Toxicology

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“…For this purpose, in the present study, two different vessels were used, mesenteric and tail arteries, which have been extensively used as models for the study of neuromodulation exerted by many substances in the vasculature [5,7,8,31–33] and where we have previously described the presence of adenosine receptors on sympathetic nerves [24,27]. …”

Section: Introductionmentioning

confidence: 99%

Endothelial and Neuronal Nitric Oxide Activate Distinct Pathways on Sympathetic Neurotransmission in Rat Tail and Mesenteric Arteries

et al. 2015

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Nitric oxide (NO) seems to contribute to vascular homeostasis regulating neurotransmission. This work aimed at assessing the influence of NO from different sources and respective intracellular pathways on sympathetic neurotransmission, in two vascular beds. Electrically-evoked [3H]-noradrenaline release was assessed in rat mesenteric and tail arteries in the presence of NO donors or endothelial/neuronal nitric oxide synthase (NOS) inhibitors. The influence of NO on adenosine-mediated effects was also studied using selective antagonists for adenosine receptors subtypes. Location of neuronal NOS (nNOS) was investigated by immunohistochemistry (with specific antibodies for nNOS and for Schwann cells) and Confocal Microscopy. Results indicated that: 1) in mesenteric arteries, noradrenaline release was reduced by NO donors and it was increased by nNOS inhibitors; the effect of NO donors was only abolished by the adenosine A1 receptors antagonist; 2) in tail arteries, noradrenaline release was increased by NO donors and it was reduced by eNOS inhibitors; adenosine receptors antagonists were devoid of effect; 3) confocal microscopy showed nNOS staining in adventitial cells, some co-localized with Schwann cells. nNOS staining and its co-localization with Schwann cells were significantly lower in tail compared to mesenteric arteries. In conclusion, in mesenteric arteries, nNOS, mainly located in Schwann cells, seems to be the main source of NO influencing perivascular sympathetic neurotransmission with an inhibitory effect, mediated by adenosine A1 receptors activation. Instead, in tail arteries endothelial NO seems to play a more relevant role and has a facilitatory effect, independent of adenosine receptors activation.

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“…9-11 Recently, our group have showed that acute resistance exercise induce an intensity-dependent effect on NO synthesis and vascular relaxation in mesenteric arteries of healthy rats. 12,13 The mesenteric artery regulates 20% of the blood flow and effectively participates in the total peripheral resistance, and thus, is directly involved in vascular changes promoted by exercise.…”

Section: Introductionmentioning

confidence: 99%

Effects of a Single Bout of Resistance Exercise in Different Volumes on Endothelium Adaptations in Healthy Animals

Mota¹,

Silva²,

Macedo³

et al. 2017

Arquivos Brasileiros De Cardiologia

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BackgroundResistance exercise (RE) has been recommended for patients with cardiovascular diseases. Recently, a few studies have demonstrated that the intensity of a single bout of RE has an effect on endothelial adaptations to exercise. However, there is no data about the effects of different volumes of RE on endothelium function.ObjectiveThe aim of the study was to evaluate the effects of different volumes of RE in a single bout on endothelium-dependent vasodilatation and nitric oxide (NO) synthesis in the mesenteric artery of healthy animals.MethodsMale Wistar rats were divided into three groups: Control (Ct); low-volume RE (LV, 5 sets x 10 repetitions) and high-volume RE (HV, 15 sets x 10 repetitions). The established intensity was 70% of the maximal repetition test. After the exercise protocol, rings of mesenteric artery were used for assessment of vascular reactivity, and other mesenteric arteries were prepared for detection of measure NO production by DAF-FM fluorescence. Insulin responsiveness on NO synthesis was evaluated by stimulating the vascular rings with insulin (10 nM).ResultsThe maximal relaxation response to insulin increased in the HV group only as compared with the Ct group. Moreover, the inhibition of nitric oxide synthesis (L-NAME) completely abolished the insulin-induced vasorelaxation in exercised rats. NO production showed a volume-dependent increase in the endothelial and smooth muscle layer. In endothelial layer, only Ct and LV groups showed a significant increase in NO synthesis when compared to their respective group under basal condition. On the other hand, in smooth muscle layer, NO fluorescence increased in all groups when compared to their respective group under basal condition.ConclusionsOur results suggest that a single bout of RE promotes vascular endothelium changes in a volume-dependent manner. The 15 sets x 10 repetitions exercise plan induced the greatest levels of NO synthesis.

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Aerobic exercise training increases neuronal nitric oxide release and bioavailability and decreases noradrenaline release in mesenteric artery from spontaneously hypertensive rats

Cited by 30 publications

References 48 publications

Impact of exercise training on redox signaling in cardiovascular diseases

Impact of exercise training on redox signaling in cardiovascular diseases

Endothelial and Neuronal Nitric Oxide Activate Distinct Pathways on Sympathetic Neurotransmission in Rat Tail and Mesenteric Arteries

Effects of a Single Bout of Resistance Exercise in Different Volumes on Endothelium Adaptations in Healthy Animals

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