Participação dos canais KATP na reatividade vascular de ratos com resistência à insulina submetidos ao exercício resistido

• Ano de defesa: 2018
• Autor(a) principal: Dantas, Cácia Oliveira
• Orientador(a): Santana-Filho, Valter Joviniano de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Programa de Pós-Graduação: Pós-Graduação em Ciências Fisiológicas
• Palavras-chave em Português: Resistência à insulina; Vasos sanguíneos; Exercícios físicos; Exercício resistido; Função vascular
• Palavras-chave em Inglês: Insulin resistance; Resistance exercise; Vascular function
• Área do conhecimento CNPq: CIENCIAS BIOLOGICAS::FISIOLOGIA
• Link de acesso: http://ri.ufs.br/jspui/handle/riufs/16681

Introduction: Insulin resistance (IR) precedes clinical manifestations of several pathological conditions. Among them stands out the vascular dysfunction that triggers damage in the vasorelaxation mechanisms. The resistance exercise (RE) promotes benefits in the cardiovascular system, one session is able to induce such benefits, thus may be a useful non-pharmacological tool to treat this dysfunction. However, the effects of a RE session on vascular dysfunction induced by IR still needs to be clarified. Objective: To investigate the effects of a moderate resistance exercise session on vascular function in animals with insulin resistance. Methods: Were used Wistar male rats (300- 350g) (CEPA/UFS 34/16). The IR induction were made through dexamethasone administration (2 mg/kg/day/i.p./7 days) in for sedentary insulin resistant (SRI) and exercised insulin resistant (ERI) groups, and saline solution 0,9% for sedentary control group (SC). The ERI group was submitted to ER protocol consisted by 5 series of 10 repetitions with 60% intensity of maximum intensity test. The systemic insulin sensibility was evaluated through insulin tolerance test (ITT) during and after induction. Following the RE session, the rats were euthanized and submitted to vascular reactivity evaluation protocol in superior mesenteric artery rings, obtaining concentration-response curves for insulin (10-13 - 10-6 mol/L) in the presence and absence of L-NAME (100 mol/L), or tetraethylammonium (TEA) (10 mol/L), or glibenclamide (GLI) (10 mol/L), or BQ 123 (10 mol/L). The results were shown as mean±EPM with two-way ANOVA test, followed by Bonferroni post-test. Results: On TTI, it was noted on the day 6 that the SC group showed preserved sensibility to insulin (35,2 mg/dL), the SRI and ERI groups had decreased sensibility (106,8 mg/dL e 108,8 mg/dL, respectively). On the day 8, the SC group still showed preserved sensibility to insulin (41 mg/dL), the SRI group still showed decreased sensibility (108,5 mg/dL), and the ERI group showed improvement in sensibility after exercise (74 mg/dL). The vasorelaxation induced by insulin in SRI group was attenuated when compared to SC group (Rmáx= 10,3 ± 0,7% vs 22,8 ± 2,2% p<0,0001) and one RE session was able to revert this attenuation (Rmáx= 23,2 ± 2,2%, p<0,0001). On pre-incubated rings with L-NAME, the vasorelaxation was almost abolished on SC group (Rmáx= 3,7 ± 1,1%, p<0,0001), while in the SRI group had a contraction (Rmáx= -4,9 ± 0,7%, p<0,0001). On the other hand, the ERI group presented increase in vasorelaxation induced by insulin when compared to SC (Rmáx= 12,1 ± 0,9 % vs. 3,7 ± 1,1%, p<0,001). Rings incubated with L-NAME+TEA the relaxation in all groups was almost abolished (SC: Rmáx= 3,7 ± 1,8% p<0,0001; SRI: Rmáx= 0,0 ± 1,4%, p<0,0001; ERI: Rmáx= 3,4 ± 0,8 %, p<0,0001). In presence of L-NAME+GLI the result was similar to L-NAME+TEA (SC: Rmáx= 3,2 ± 1,0% p<0,0001; SRI: Rmáx= 0,4 ± 0,9%, p<0,0001; ERI: Rmáx= 3,6 ± 0,8 %, p<0,0001). With L-NAME+BQ 123, the groups SC and SRI had their relaxation abolished (SC: Rmáx= 2,2 ± 1,1% p<0,0001; SRI: Rmáx= 0,1 ± 1,3%, p<0,0001), however, the ERI group showed relaxation (Rmáx= 10,4 ± 1,4 %, p<0,0001). Conclusion: Our results suggest that one session of ER with moderate intensity is able to promote adjusts in the vascular dysfunction caused by IR through NO dependent mechanisms and K+ channels subtype KATP.