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

• Main Authors: Joel Alves Rodrigues, Thales Nicolau Prímola-Gomes, Leôncio Lopes Soares, Tiago Ferreira Leal, Clara Nóbrega, Danillo Laviola Pedrosa, Leonardo Mateus Teixeira Rezende, Edilamar Menezes de Oliveira, Antonio Jose Natali
• Format: Article
• Language: English
• Published: Sociedade Brasileira de Cardiologia (SBC) 2018-07-01
• Series: Arquivos Brasileiros de Cardiologia
• Subjects: Hypertension; Exercise; Rats; Calcium Signaling; Intracellular Calcium; Sensing Proteins
• Online Access: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2018001400172&lng=en&tlng=en

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.