Exercise training restores the endothelial progenitor cells number and function in hypertension

Fernandes, Tiago; Nakamuta, Juliana Sanajotti; Magalhães, Flávio de Castro; Roque, Fernanda Roberta; Lavini-Ramos, Carolina; Schettert, Isolmar Tadeu; Coelho, Verônica; Krieger, José Eduardo; Oliveira, Edilamar Menezes de

doi:10.1097/hjh.0b013e3283588d46

Cited by 68 publications

(74 citation statements)

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“…Increase of the pro-apoptotic activity of Bad in SHR was confirmed, since we verified decrease of phosphorylated Bad in Ser112 and of p-Bad ser112 /Bad ratio. Moreover, our results showed that reduction of endothelial NO synthesis followed by increase in protein expression of iNOS could contribute to moderate exchange of redox homeostasis towards a pro-oxidant status, corroborating for the activation of the microvascular pro-apoptotic signaling way since the oxidative stress mediated by hypertension harms the vasodilator response and apoptosis of the endothelial cell associated with loss of microvessels 13,14,30 . Consistent to the data in the literature, ET restored the VEGF levels followed by increase in expression of VEGFR2.…”

Section: Discussionsupporting

confidence: 70%

O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

Fernandes

Magalhães

Carmo

et al. 2012

Rev Bras Med Esporte

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Aerobic exercise training (ET) has been established as an important non-pharmacological treatment for hypertension, since it corrects the microvascular rarefaction and decreases blood pressure. Studies have shown that microvascular abnormalities are directly associated with changes in the vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2), as well as with imbalance of apoptotic signaling in hypertension. However, little is known about these mechanisms in hypertension. We hypothesized that ET restores angiogenic factors and promotes balance between anti and pro-apoptotic proteins of the Bcl-2 family, potentially contributing to revascularization and the disease regression. Twelve-week old male Spontaneously Hypertensive Rats (SHR, n=14) and Wistar Kyoto Rats (WKY, n=14) were randomly assigned into 4 groups: SHR, trained SHR (SHR-T), WKY and trained WKY (WKY-T) were studied. As expected, ten weeks of ET were effective in reducing blood pressure in SHR-T group. In addition, ET promoted resting bradycardia in trained groups (WKY-T and SHR-T), being considered an important marker of aerobic ET. ET has also corrected the capillary rarefaction in SHR-T and this response is partly due to recovery of the peripheral levels of VEGF and increase in VEGFR2 expression. Concomitantly, normalization of the apoptotic pathway was observed, with increased expression of the anti-apoptotic proteins (Bcl-2 and Bcl-x) and reduction of the pro-apoptotic protein (Bad), followed by phosphorylation of the Bad protein and decrease in the Bad/Bcl-x association. These data suggest that ET promotes peripheral revascularization in hypertension dependent on a fine balance between positive and negative regulators of angiogenesis.

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Section: Discussionsupporting

confidence: 70%

O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

Fernandes

Magalhães

Carmo

et al. 2012

Rev Bras Med Esporte

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“…Angiogenesis is a key determinant of skeletal muscle function, and previous reports in animal models and humans have shown a beneficial effect of physical exercise on factors that sustain capillarization levels in skeletal muscles (Fernandes et al 2012;Shibuya 2013). In this context, we found that the vascular endothelial growth factor A (Vegfa) was significantly increased by WR in fP8WR female mice, while no change was detected in fR1CON controls (Fig.…”

Section: Impact Of Wheel Running In the Expression Of Skeletal Musclesupporting

confidence: 55%

Long-term wheel running changes on sensorimotor activity and skeletal muscle in male and female mice of accelerated senescence

Sanchez‐Roige

Lalanza

Álvarez-López

et al. 2014

AGE

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The senescence-accelerated mouse prone 8 (SAMP8) is considered a useful non-transgenic model for studying aspects of aging. Using SAM resistant 1 (SAMR1) as controls, the long-term effects of wheel running on skeletal muscle adaptations and behavioral traits were evaluated in senescent (P8) and resistant (R1) male and female mice. Longterm wheel running (WR) led to increases in locomotor activity, benefits in sensorimotor function, and changes in body weight in a gender-dependent manner. WR increased body weight and baseline levels of locomotor activity in female mice and improved balance and strength in male mice, compared to sedentary-control mice. WR resulted in key metabolic adaptations in skeletal muscle, associated with an increased activity of the sirtuin 1-AMP-activated protein kinase (AMPK)-PGC-1 alpha axis and changes in vascular endothelial growth factor A (Vegfa), glucose transporter type 4 (Glut4), and Cluster of Differentiation 36 (Cd36) gene expression. Overall, our data indicate that activity, balance, and strength decrease with age and that long-term WR may significantly improve the motor function in a mouse model of senescence in a gender-dependent manner.

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“…This is not entirely surprising as it has been reported that functional sympatholysis is mediated by NO in normotensive humans and animals (8,10,15,17,56). Recent evidence suggests that protein levels for endothelial NOS in the soleus muscle of SHR are significantly lower compared with WKY (18). Decreases in NOS expression could mediate reductions in the availability of NO within skeletal muscle in hypertension and may potentially account for the blunting of functional sympatholysis in hypertensive animals.…”

Section: Impairments In Functional Sympatholysis In Shrmentioning

confidence: 93%

Exercise training improves functional sympatholysis in spontaneously hypertensive rats through a nitric oxide-dependent mechanism

Mizuno

Iwamoto

Vongpatanasin

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Mizuno M, Iwamoto GA, Vongpatanasin W, Mitchell JH, Smith, SA. Exercise training improves functional sympatholysis in spontaneously hypertensive rats through a nitric oxide-dependent mechanism. Am J Physiol Heart Circ Physiol 307: H242-H251, 2014. First published May 9, 2014; doi:10.1152/ajpheart.00103.2014.-Functional sympatholysis is impaired in hypertensive animals and patients. Exercise training (ET) improves functional sympatholysis through a nitric oxide (NO)-dependent mechanism in normotensive rats. However, whether ET has similar physiological benefits in hypertension remains to be elucidated. Thus we tested the hypothesis that the impairment in functional sympatholysis in hypertension is reversed by ET through a NO-dependent mechanism. In untrained normotensive Wistar-Kyoto rats (WKY UT; n ϭ 13), untrained spontaneously hypertensive rats (SHRUT; n ϭ 13), and exercise-trained SHR (SHRET; n ϭ 6), changes in femoral vascular conductance (FVC) were examined during lumbar sympathetic nerve stimulation (1, 2.5, and 5 Hz) at rest and during muscle contraction. The magnitude of functional sympatholysis (⌬%FVC ϭ ⌬%FVC muscle contraction Ϫ ⌬%FVC rest) in SHR UT was significantly lower than WKYUT (1 Hz: Ϫ2 Ϯ 4 vs. 13 Ϯ 3%; 2.5 Hz: 9 Ϯ 3 vs. 21 Ϯ 3%; and 5 Hz: 12 Ϯ 3 vs. 26 Ϯ 3%, respectively; P Ͻ 0.05). Three months of voluntary wheel running significantly increased maximal oxygen uptake in SHRET compared with nontrained SHRUT (78 Ϯ 6 vs. 62 Ϯ 4 ml·kg Ϫ1 ·min Ϫ1 , respectively; P Ͻ 0.05) and restored the magnitude of functional sympatholysis in SHR ET (1 Hz: 9 Ϯ 2%; 2.5 Hz: 20 Ϯ 4%; and 5 Hz: 34 Ϯ 5%). Blockade of NO synthase (NOS) by N G -nitro-L-arginine methyl ester attenuated functional sympatholysis in WKYUT but not SHR UT. Furthermore, NOS inhibition significantly diminished the improvements in functional sympatholysis in SHRET. These data demonstrate that impairments in functional sympatholysis are normalized via a NO mechanism by voluntary wheel running in hypertensive rats.

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Exercise training restores the endothelial progenitor cells number and function in hypertension

Abstract: Our data show that exercise training repairs the impairment of EPC in hypertension, which could be associated with peripheral revascularization, suggesting a mechanism for its potential therapeutic application in vascular diseases.

Cited by 68 publications

References 44 publications

O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

O treinamento físico aeróbio inibe a sinalização apoptótica muscular esquelética mediada por VEGF-VEGR2 em ratos espontaneamente hipertensos

Long-term wheel running changes on sensorimotor activity and skeletal muscle in male and female mice of accelerated senescence

Exercise training improves functional sympatholysis in spontaneously hypertensive rats through a nitric oxide-dependent mechanism

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