Swimming training promotes cardiac remodeling and alters the expression of mRNA and protein levels involved in calcium handling in hypertensive rats Jamille Locatelli a,b, ⁎, Leonardo Vinícius Monteiro de Assis c , Carolina Morais Araújo a , Andréia Carvalho Alzamora a,d,e , Wanderson Geraldo de Lima a,d , Maria José Campagnole-Santos e,f , Robson Augusto dos Santos e,f , Mauro César Isoldi a,d a Center for Research in Biological Sciences, Federal University of Ouro Preto, Ouro Preto, Brazil b Sports Center, Federal University of Ouro Preto, Ouro Preto, Brazil c Departament of Physiology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil d Department of Biological Science, Institute of Exact and Biological Sciences, Ouro Preto, Brazil e National Institute of Science and Technology in Nano-Biopharmaceutical Innovation, Belo Horizonte, Brazil f Departament of Physiology and Biophysics, Institute of Biological Science, Federal University of Minas Gerais, Belo Horizonte, Brazil abstract article info Article history: Received 6 February 2014 Accepted 20 September 2014 Available online 2 October 2014 Keywords: Calcium handling Renovascular hypertension Swimming Cardiac hypertrophy Aim: The aim of this study was to identify the effects of swimming training on the mRNA expression and protein levels of the calcium handling proteins in the hearts of renovascular hypertensive rats submitted to swimming protocol during 6 weeks. Main methods: Fischer rats with renovascular hypertension 2-kidney 1-clip (2K1C) and SHAM groups were divid- ed among sedentary and exercised groups. The exercise protocol lasted for 6 weeks (1 h/day, 5×/week), and the mean arterial pressure, cardiomyocytes hypertrophy parameters, mRNA expression and protein levels of some calcium handling proteins in the left ventricle were evaluated. Key findings: Swimming training was able to reduce the levels of mean arterial pressure in the hypertensive group compared to 2K1C SED, and to promote cardiac hypertrophy in SHAM EX and 2K1C EX groups in comparison to the respective control groups. The mRNA levels of B-type natriuretic peptide were reduced in the 2K1C EX when compared to 2K1C SED. The mRNA and protein levels of the sarcoplasmic reticulum Ca 2+ -ATPase increased after the swimming training in SHAM and 2K1C groups. The mRNA and protein levels of phospholamban, displayed an increase in their levels in the exercised SHAM and in hypertensive rats in comparison to their respective controls; while mRNA levels of Na + /Ca 2+ exchanger was reduced in the left ventricle comparing to the sedentary hyper- tensive rats. Significance: Taken altogether, we provide evidence that the aerobic training may lead to cardiac remodeling, and modulate the calcium handling proteins expression in the heart of hypertensive rats. © 2014 Elsevier Inc. All rights reserved. Introduction Hypertension is a multifactorial disease that involves interactions between the genetically driven homeostatic control mechanisms and environmental factors (Takahashi and Smithies, 2004). It is estimated that 1 billion people worldwide have hypertension, representing a seri- ous worldwide public health problem mainly because hypertension is a major and well known risk factor for cardiovascular diseases. Several treatment guidelines, pharmacological (Edwards et al., 2014) and non-pharmacological approaches, such as physical exercise (Semlitsch et al., 2013) have been suggested in order to maintain the blood pres- sure at acceptable levels. It is well known that physical exercise is able to reduce the blood pressure levels or even to delay the onset of hypertension in rats with Goldblatt hypertension (Rodrigues et al., 2007; Soares et al., 2011), which is an experimental model dependent on the renin–angiotensin system (RAS) that controls blood pressure in renovascular hyperten- sion. The increase in the activity of this system may lead to hypertension (Reckelhoff et al., 2000), and may also cause deleterious effects on the heart, such as reduction on the Ca 2+ transient (Kemi et al., 2007). The Angiotensin II (Ang II) is an octapeptide produced from the sub- strate angiotensinogen through sequential enzymatic cleavages by renin and angiotensin converting enzyme (ACE). This peptide is the Life Sciences 117 (2014) 67–74 ⁎ Corresponding author at: Center for Research in Biological Sciences, Federal University of Ouro Preto, Morro do Cruzeiro, Zip Code 35400-000, Ouro Preto, MG, Brazil. Tel.: +55 31 3559 1693. E-mail address: jahefi@hotmail.com (J. Locatelli). http://dx.doi.org/10.1016/j.lfs.2014.09.024 0024-3205/© 2014 Elsevier Inc. All rights reserved. Contents lists available at ScienceDirect Life Sciences journal homepage: www.elsevier.com/locate/lifescie