Programa de Pós-graduação em Ciências Fisiológicas - Multicêntrico
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Item 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(Universidade Federal de Goiás, 2023-07-26) Dias, Matheus Lobo Perez; Custódio, Carlos Henrique Xavier; http://lattes.cnpq.br/0207928273284808; Pedrino, Gustavo Rodrigues; http://lattes.cnpq.br/1155446449250341; Pedrino, Gustavo Rodrigues; Rosa, Daniel Alves; Pansani, Aline PriscilaThe 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 XX 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.Item Contribuição dos aferentes sinoaórticos nos ajustes renais, cardiovasculares, simpáticos e ventilatórios induzidos por hiperosmolalidade aguda(Universidade Federal de Goiás, 2017-01-20) Silva, Elaine Fernanda da; Colombari, Eduardo; http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4721289A2; Pedrino, Gustavo Rodrigues; http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4762065Z5; Braga, Valdir de Andrade; Silveira, Nusa de Almeida; Ferreira, Patrícia Maria; Castro, Carlos Henrique de; Colombari, EduardoThe forebrain is suggested the main sensorial site for monitoring changes in plasma osmolality. In addition to the central mechanisms, it has been suggested that peripheral sensors may participate in the osmoregulation. In the present study we investigated the contribution of the sinoaortic afferents in the physiological mechanisms of regulation of the body fluids tonicity during acute hyperosmolality. In the first part of the study, we explored the participation of sinoaortic afferents in the cardiovascular, renal and autonomic responses induced by hypernatremia. Wistar rats (280-350 g) were anesthetized with halothane (2% in O2) and submitted to sinoaortic denervation (SAD), carotid body removal (CBX) or fictitious surgery, and implantation of cannula in the right femoral artery and vein to blood pressure (BP) recording and substance administration, respectively. In the next day, SAD animals were anesthetized with urethane (1.2 g/kg body weight, i.v.) and instrumentalized for renal sympathetic nerve activity (rSNA) recording. Non-anaesthetized CBX animals were used to BP recording and renal excretion test. The parameters were evaluated in response to intravenous infusion of hypertonic saline (HS) (3 mol/L NaCl, 1.8 mL/kg body weight, in 60 seconds). Renal sympathoinhibition induced by infusion of HS was abolished in SAD rats (SAD: -10.7 ± 5.5% of baseline, vs. control rats: -28.7 ± 4.8% of baseline, 60 minutes after HS, p<0.05). CBX attenuated the pressor response (CBX: 5.7 ± 2.0 mmHg, vs. control: 15.8 ± 2.0 mmHg, 12 minutes after HS; p<0.05) and sodium renal excretion (CBX: 74.9 ± 7.3%, vs. control: 99.7 ± 6.7%, 90 minutes after HS; p<0.05) to HS. These results show that the integrity of the aortic and carotid afferents are essential for autonomic, cardiovascular and renal adjustments induced by acute hypernatremia. In the second part we explored the involvement of the carotid bodies and forebrain in the autonomic and ventilatory responses induced by intra arterial infusion of HS using arterially-perfused in situ rat preparations (male Holtzman rats, 60-100 g). HS infusions (0.17; 0.3; 0.7; 1.5 and 2 mol/L NaCl; 200 µL during 20 seconds each) were performed in accumulative ascending order while thoracic sympathetic, phrenic and carotid sinus nerve activities were recorded. Intra-arterial infusion of 2 mol/L NaCl, produced a modest increase in phrenic burst frequency (5.8 ± 0.9 bpm, vs. Ringer: 0.4 ± 0.2 bpm, p<0.05) and markedly enhanced sympathetic (63.3 ± 8.4%, vs. Ringer: -0.8 ± 1.9%, p<0.05) and carotid sinus nerve activities (105.1 ± 13.2%, vs. Ringer: -0.2 ± 1.3%, p<0.05). Carotid bodies removal attenuated the sympathoexcitation (26.2 ± 4.9%, p<0.05), but not the tachypnea (3.6 ± 0.5 bpm) induced by 2 mol/L NaCl. The forebrain disconnection at the pre-collicular level, abolished the sympathoexcitation (8.4 ± 3.7%, p<0.05) and the increase in phrenic burst frequency (1.2 ± 0.4 bpm, p<0.05) in response to 2 mol/L NaCl. The results indicate the participation of forebrain in the sympathetic and ventilatory responses produced by sodium overload. Moreover, they suggest that carotid bodies may act as a sodium peripheral sensor contributing for the autonomic responses to acute hyperosmotic challenges.