Efeitos do treinamento físico aeróbico sobre as respostas cardiovasculares e autonômicas induzidas pela estimulação do processo neuroinflamatório em ratos espontaneamente hipertensos: enfoque no núcleo paraventricular hipotalâmico
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2023-07-26
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Universidade Federal de Goiás
Resumo
The autonomic nervous system (ANS) comprises the sympathetic nervous system
(SNS) and the parasympathetic nervous system (PSNS), which are associated with
the regulation of the cardiovascular function. Neuroinflammation and the increase of
the sympathetic tone are reported as angular stone in the genesis of the arterial
hypertension (AH), which is the main factor for modifiable risk for the problem
associated with development, maintenance and aggravation in the cardiovascular
diseases (CVD). The sympathetic flow is modulated by different elemental nucleus
located in the central nervous system (CNS), such as the hypothalamic paraventricular
nucleus (PVN) and the rostral ventrolateral medulla (RVLM). Conditions circumscribed
to these regions are frequently implicated to the autonomic imbalance, driving force in
pathogenesis of the AH. Although the neurons in these cardiovascular and autonomic
central control regions contribute to the modulation of the sympathetic flow, the factors
that cooperate to the increase of the neuron activity are still under investigation. In the
last decades, many experimental evidence related the brain cytokines to the autonomic
imbalance observed in different models of AH. The tumor necrosis factor alpha (TNFα) is a constituent of the pro-inflammatory cytokines (PICs) that acts as
neuromodulator and perform a fundamental role in the sympathetic regulation of the
blood pressure (BP). Studies suggest that the increase of the PICs expression
activates many signaling ways and acutely influence the neural discharge, promoting
adaptative changes that modulate the neuronal excitability through genic transcription.
On the other hand, the aerobic physical training (APT) is recognized as a preventive
and adjuvant therapeutic too in AH management. In light of these considerations, the
present study evaluated the contribution of the neuroinflammatory process to the
cardiovascular and autonomic responses induced by TNF-α in the PVN of hypertensive
animals undergoing a regular moderate-intensity APT protocol. To this end, SHR (250
- 350g) were divided into two groups: I. SHR-APT (8 weeks of aerobic training, n=13);
II. SHR-SED (8 weeks of supervision in species-typical physical activity, n=10). The
systolic blood pressure (SBP) and the heart rate (HR) was monitored throughout the
whole treatment period with the tail plethysmography (TP). At the end of the 8 weeks,
the animals were anesthetized with urethane (400 mg·kg−1 body weight; i.v.)
associated with α-chloralose (40 mg·kg−1 body weight; i.v.) and surgically instrumented
for unilateral intranuclear nanoinjections (50nL) in the PVN, recording of mean arterial
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pressure (MAP), HR and splanchnic sympathetic nerve activity (SSNA). During the
non-anesthetized records, we identified that the APT promoted resting bradycardia
observed from the 3rd week of training (SHR-APT: from 488,9 ± 13,1 to 450,2 ± 11,6
bpm; p<0,05). In the fraction of the study where the recordings were performed in
anesthetized SHR, we identified that the vehicle nanoinjections (phosphate-buffered
saline; PBS, 0.01 M) in the PVN didn’t promote the change in the basal values of the
MAP (SHR-SED: Δ -2,1 ± 1,3; SHR-APT: Δ -0,7 ± 1,4 mmHg; 10 min after vehicle,
from baseline), HR (SHR-SED: Δ 0,039 ± 1,6; SHR-APT: Δ -1,0 ± 1,8 bpm; 10 min
after vehicle, from baseline) and ∫SSNA (SHR-SED: Δ +9,7 ± 2,0; SHR-APT: Δ +4,3 ±
1,7%; 10 min after vehicle, from baseline), in the same way that it wasn’t observed
differences between the groups. In the other hand, intranuclear nanoinjections of TNFα in the PVN of hypertensive animals that remained in species-typical physical activity
induced an increase in MAP (SHR-SED: Δ +11,4 ± 3,9 mmHg; p<0,05; 50 min after
TNF-α, from baseline), HR (SHR-SED: Δ +18.8 ± 4.5 bpm; p<0.05; 60 min after TNFα, from baseline) and ∫SSNA (SHR-SED: Δ +21.8 ± 4.7 %; p<0.05, 20 min after TNFα, from baseline). In SHR submitted to APT, we found that nanoinjections of TNF-α
into the PVN did not elicit pressor responses (SHR-TFA: Δ -4.6 ± 2.4 vs. SHR-SED: Δ
+6.8 ± 4.2 mmHg; p<0.05; 40 min after TNF-α), nor did they result in sympathetic
excitation (SHR-SED: Δ +30.6 ± 4.7 vs. SHR-TFA: Δ +14.3 ± 4.9 %; p<0.05; 30 min
after TNF-α), as observed in the sedentary group. Additionally, there was a significant
difference in these parameters when comparing the training groups to the sedentary
groups of animals. Taken together, our findings demonstrate that regularly performed
moderate-intensity APT effectively promotes resting bradycardia while also mitigating
the increase in SSNA and pressor response induced by acute activation of the
neuroinflammatory process in the PVN of SHR.
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PEREZ, M. L. D. Efeitos do treinamento físico aeróbico sobre as respostas cardiovasculares e autonômicas induzidas pela estimulação do processo neuroinflamatório em ratos espontaneamente hipertensos: enfoque no núcleo paraventricular hipotalâmico. 2023. 59 f. Dissertação (Mestrado em Ciências Fisiológicas) - Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, 2023.