Caracterização das alterações hemodinâmicas ocasionadas pelo reflexo pressórico ao exercício em ratos normotensos e hipertensos: participação do RVLM e possíveis mecanismos periféricos

• Autor(a) principal: Silveira, Laíla Milhomem
• Data de Publicação: 2019
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFG
• Texto Completo: http://repositorio.bc.ufg.br/tede/handle/tede/10053
• topic: Reflexo pressórico ao exercício; SHR; Sistema nervoso autonômico; Sistema cardiovascular; Exercise pressure reflex; Autonomic nervous system; Cardiovascular system; CIENCIAS BIOLOGICAS::FISIOLOGIA

Static muscle contraction promotes an increase in blood pressure (BP) and heart rate (HR) by means of a peripheral neural reflex of muscular origin, the " exercise reflex pressure" (EPR). It is well established in the literature that cardiovascular adjustments in responses to physical exercise are altered in hypertensive individuals, and some of these alterations are attributed to the central mechanisms - associated with mismatches in the autonomic sympathetic component - as well as the peripheral mechanisms characterized by vascular endothelial dysfunction. The rostralventrolateral region of the medulla (RVLM) is the main efferent arm of vasomotor neurons for tonic maintenance and BP reflex. Experimental evidence indicates the participation of RVLM in HR and BP increase induced by EPR. However, little is known about its participation in this reflex, regarding hemodynamic adjustments, such as alteration in blood flow (BF) and aortic (AVC) and renal vascular conductance (RVC), of normotensive and hypertensive animals. Objective: investigate the central role of RVLM and peripheral vasodilator mechanisms in hemodynamic changes resulting from EPRevocated by the static muscle contraction of the sural triceps by tibial nerve electrical stimulation (TNES) in WISTAR and spontaneously hypertensive rats(SHR). Methodology: Wistars (n = 10) and SHR (n = 6) (250-350g) were anesthetized and instrumented to record BP, HR, ABF, RBF, AVC and RVC. The left sural triceps tendon was attached to a force transducer to measure the developed muscle tension. The tibial nerve was stimulated by electrical current for 30 s at a frequency of 40Hz, 0.1 ms pulse duration and 5x motor threshold. The TNES was performed before and after quinurenic acid nanoinjection (KYN, 50 nL) in the contralateral RVLM to the stimulated nerv. The injection site was targed, and its medulla was removed for histological analysis. In a later protocol, SHRs (treated SHR, n = 7) were treated with Nebivolol Hydrochloride (NBL, 10mg / kg) or distilled water (control SHR, n = 5) for 15 days by gavage. They were then submitted to the same experimental procedures as the initial protocol, except for the central nanoinjection. Data were expressed as mean +/- SEM and Student's t-test and One-way ANOVA tests were used. P ≤ 0.05.RESULTS: In WISTARs and SHRs, EPR evocated byTNES increased BP and HR, which were reduced after KYNnanoinjection in RVML. In WISTARs, EPR caused increase in ABF and AVC, IX butafter the injection in the contralateral RVLM, we noticed a reduction in this response. In SHR, there were no changes of ABF or AVC during contractions, before and after glutamatergic blockade. In WISTAR animals, EPR produced RBF and RVC reduction during TNES. After the glutamatergic blockade in RVLM, however, the RBF and RVC responses were not altered. The EPR in SHR did not trigger RBF and RVC reduction, as well KYN in RVLM. The 15-day NBL treatment did not alter the SHRs AVC and RVC changes. CONCLUSION: BP and HR responses induced by TNES were reduced with glutamatergic blockade in RVLM in WISTARs and SHRs. In WISTARs, TNES was associated with aortic vasodilation and renal vasoconstriction. This response differs in SHRs, where we did not observe ABF and AVC changes (CONTROL or POST-KYN). Thus, we demonstrate that in the EPR, ABF, RBF, AVC, and RVC responses of normotensive and spontaneously hypertensive rats are distinct, and contralateral RVLM to the active musculature of these animals, participates in the responses of aortic vasodilation and renal vasoconstriction in normotensive rats, but does not significantly influence BF variations in SHR. In addition, the 15-day treatment with the nitric oxide (NO) donor and NBL selective beta blocker was also not able to alter the hemodynamic responses in SHRs.