Artigo Acesso aberto Produção Nacional Revisado por pares

Physical Exercise and Regulation of Intracellular Calcium in Cardiomyocytes of Hypertensive Rats

2018; Sociedade Brasileira de Cardiologia (SBC); Linguagem: Inglês

10.5935/abc.20180113

ISSN

1678-4170

Autores

Joel Alves Rodrigues, Thales Nicolau Prímola‐Gomes, Leôncio Lopes Soares, Tiago Ferreira Leal, Clara Nóbrega, Danillo Laviola Pedrosa, Leonardo Mateus Teixeira de Rezende, Edilamar Menezes de Oliveira, Antônio José Natali,

Tópico(s)

Adipose Tissue and Metabolism

Resumo

Background: Regulation of intracellular calcium (Ca2+) in cardiomyocytes is altered by hypertension; and aerobic exercise brings benefits to hypertensive individuals. Objective: To verify the effects of aerobic exercise training on contractility and intracellular calcium (Ca2+) transients of cardiomyocytes and on the expression of microRNA 214 (miR-214) in the left ventricle of spontaneously hypertensive rats (SHR). Methods: SHR and normotensive Wistar rats of 16 weeks were divided into 4 groups -sedentary hypertensive (SH); trained hypertensive (TH); sedentary normotensive (SN); and trained normotensive (TN). Animals of the TH and TN groups were subjected to treadmill running program, 5 days/week, 1 hour/day at 60-70% of maximum running velocity for 8 weeks. We adopted a p ≤ 0.05 as significance level for all comparisons. Results: Exercise training reduced systolic arterial pressure in hypertensive rats. In normotensive rats, exercise training reduced the time to 50% cell relaxation and the time to peak contraction and increased the time to 50% decay of the intracellular Ca2+ transients. In SHR, exercise increased the amplitude and reduced the time to 50% decay of Ca2+ transients. Exercise training increased the expression of miR-214 in hypertensive rats only. Conclusion: The aerobic training applied in this study increased the availability of intracellular Ca2+ and accelerated the sequestration of these ions in left ventricular myocytes of hypertensive rats, despite increased expression of miR-214 and maintenance of cell contractility.

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