Endothelium adjustments to acute resistance exercise are intensity-dependent in healthy animals

Mota, Marcelo Mendonça; Mesquita, Thássio; Silva, Tharciano Luiz Teixeira Braga da; Fontes, Milene Tavares; Lauton-Santos, Sandra; Capettini, Luciano dos Santos Aggum; Jesus, Itamar Couto Guedes de; Quintans‐Júnior, Lucindo José; Angelis, Kátia De; Wichi, Rogério Brandão; Santos, Márcio Roberto Viana dos

doi:10.1016/j.lfs.2015.10.007

Cited by 19 publications

(23 citation statements)

References 32 publications

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“…Western blots were performed as previously described (Mota et al, 2015), with some modifications. Thirty to fifty microgram of protein were resolved on SDS–PAGE, transferred to a PVDF membrane, and incubated with the following primary antibodies: anti-eNOS (1:1000, sc-654), anti-nNOS (1:1000, sc-8309), M 2 (1:1000, sc-9107) anti-peNOS ser1177 (1:1000, sc-12972), anti-pnNOS ser852 (1:1000, sc-19826), anti-SERCA2 (1:2500, sc-376235), and anti-GAPDH (1:3000, sc-32233) from Santa Cruz Biotechnology or β 1 -AR (1:1000, ab3442, Abcam).…”

Section: Methodsmentioning

confidence: 99%

Cardioprotective Action of Ginkgo biloba Extract against Sustained β-Adrenergic Stimulation Occurs via Activation of M2/NO Pathway

et al. 2017

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Ginkgo biloba is the most popular phytotherapic agent used worldwide for treatment of several human disorders. However, the mechanisms involved in the protective actions of Ginkgo biloba on cardiovascular diseases remain poorly elucidated. Taking into account recent studies showing beneficial actions of cholinergic signaling in the heart and the cholinergic hypothesis of Ginkgo biloba-mediated neuroprotection, we aimed to investigate whether Ginkgo biloba extract (GBE) promotes cardioprotection via activation of cholinergic signaling in a model of isoproterenol-induced cardiac hypertrophy. Here, we show that GBE treatment (100 mg/kg/day for 8 days, v.o.) reestablished the autonomic imbalance and baroreflex dysfunction caused by chronic β-adrenergic receptor stimulation (β-AR, 4.5 mg/kg/day for 8 days, i.p.). Moreover, GBE prevented the upregulation of muscarinic receptors (M2) and downregulation of β1-AR in isoproterenol treated-hearts. Additionally, we demonstrated that GBE prevents the impaired endothelial nitric oxide synthase activity in the heart. GBE also prevented the pathological cardiac remodeling, electrocardiographic changes and impaired left ventricular contractility that are typical of cardiac hypertrophy. To further investigate the mechanisms involved in GBE cardioprotection in vivo, we performed in vitro studies. By using neonatal cardiomyocyte culture we demonstrated that the antihypertrophic action of GBE was fully abolished by muscarinic receptor antagonist or NOS inhibition. Altogether, our data support the notion that antihypertrophic effect of GBE occurs via activation of M2/NO pathway uncovering a new mechanism involved in the cardioprotective action of Ginkgo biloba.

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Section: Methodsmentioning

confidence: 99%

Cardioprotective Action of Ginkgo biloba Extract against Sustained β-Adrenergic Stimulation Occurs via Activation of M2/NO Pathway

et al. 2017

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“…Similarly, Mota et al. 13 observed that high-intensity resistance exercise enhanced the relaxation induced by insulin in mesenteric artery of healthy animals. Thus, we hypothesize that both, high-volume and -intensity, are linked with enhanced vascular function.…”

Section: Discussionmentioning

confidence: 82%

“…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. 9 …”

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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“…NO· production in the aorta was determined using a fluorescent cell-permeable dye, 4,-amino-5 methylamino-2′,7′-diaminofluorescein diacetate (DAF-FM, 10 μM; Molecular Probes) as previously described (Mota et al, 2015). Intracellular superoxide levels were assessed using dihydroethidium (DHE, 10 μM; Calbiochem).…”

Section: Methodsmentioning

confidence: 99%

Vascular Kinin B1 and B2 Receptors Determine Endothelial Dysfunction through Neuronal Nitric Oxide Synthase

et al. 2017

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B1- and B2-kinin receptors are G protein-coupled receptors that play an important role in the vascular function. Therefore, the present study was designed to evaluate the participation of kinin receptors in the acetylcholine (ACh)-induced vascular relaxation, focusing on the protein-protein interaction involving kinin receptors with endothelial and neuronal nitric oxide synthases (eNOS and nNOS). Vascular reactivity, nitric oxide (NO·) and reactive oxygen species (ROS) generation, co-immunoprecipitation were assessed in thoracic aorta from male wild-type (WT), B1- (B1R−/−), B2- (B2R−/−) knockout mice. Some vascular reactivity experiments were also performed in a double kinin receptors knockout mice (B1B2R−/−). For pharmacological studies, selective B1- and B2-kinin receptors antagonists, NOS inhibitors and superoxide dismutase (SOD) mimetic were used. First, we show that B1- and B2-kinin receptors form heteromers with nNOS and eNOS in thoracic aorta. To investigate the functionality of these protein-protein interactions, we took advantage of pharmacological tools and knockout mice. Importantly, our results show that kinin receptors regulate ACh-induced relaxation via nNOS signaling in thoracic aorta with no changes in NO· donor-induced relaxation. Interestingly, B1B2R−/− presented similar level of vascular dysfunction as found in B1R−/− or B2R−/− mice. In accordance, aortic rings from B1R−/− or B2R−/− mice exhibit decreased NO· bioavailability and increased superoxide generation compared to WT mice, suggesting the involvement of excessive ROS generation in the endothelial dysfunction of B1R−/− and B2R−/− mice. Alongside, we show that impaired endothelial vasorelaxation induced by ACh in B1R−/− or B2R−/− mice was rescued by the SOD mimetic compound. Taken together, our findings show that B1- and B2-kinin receptors regulate the endothelium-dependent vasodilation of ACh through nNOS activity and indicate that molecular disturbance of short-range interaction between B1- and B2-kinin receptors with nNOS might be involved in the oxidative pathogenesis of endothelial dysfunction.

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Endothelium adjustments to acute resistance exercise are intensity-dependent in healthy animals

Cited by 19 publications

References 32 publications

Cardioprotective Action of Ginkgo biloba Extract against Sustained β-Adrenergic Stimulation Occurs via Activation of M2/NO Pathway

Cardioprotective Action of Ginkgo biloba Extract against Sustained β-Adrenergic Stimulation Occurs via Activation of M2/NO Pathway

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

Vascular Kinin B1 and B2 Receptors Determine Endothelial Dysfunction through Neuronal Nitric Oxide Synthase

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