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

• Autor(a) principal: Rodrigues,Joel Alves
• Data de Publicação: 2018
• Outros Autores: Prímola-Gomes,Thales Nicolau, Soares,Leôncio Lopes, Leal,Tiago Ferreira, Nóbrega,Clara, Pedrosa,Danillo Laviola, Rezende,Leonardo Mateus Teixeira, Oliveira,Edilamar Menezes de, Natali,Antonio Jose
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Arquivos Brasileiros de Cardiologia (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2018001400172
• topic: Hypertension; Exercise; Rats; Calcium Signaling; Intracellular Calcium; Sensing Proteins

Abstract 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.