Exp Physiol 93.5 pp 589–598 589 Experimental Physiology Selective increase of angiotensin(1–7) and its receptor in hearts of spontaneously hypertensive rats subjected to physical training Ary Gomes Filho 1 , Anderson J. Ferreira 2 ,S´ ergio Henrique S. Santos 1 , S´ ılvia R. S. Neves 2 , Elizabeth R. Silva Camargos 2 , Lenice K. Becker 1 , Hindiael A. Belchior 1 , Marco Fabricio Dias-Peixoto 1 , S´ ergio V. B. Pinheiro 1 and Robson A. S. Santos 1 Departments of 1 Physiology and Biophysics and 2 Morphology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil In the present study we investigated the effects of physical training on plasma and cardiac angiotensin(1–7) [Ang(1–7)] levels. In addition, possible changes in expression of the Ang(1–7) Mas receptor in the heart were also evaluated. Normotensive Wistar rats and spontaneously hypertensive rats (SHR) were subjected to an 8 week period of 5% overload swimming training. Blood pressure was determined by a tail-cuff system. Heart and left ventricle weights and cardiomyocyte diameter were analysed to evaluate cardiac hypertrophy. Radioimmunoassay was used to measure angiotensin levels. Expression of Mas was determined by semi-quantitative polymerase chain reaction, immunofluorescence and Western blotting. Physical training induced cardiac hypertrophy in Wistar rats and SHR. A significant decrease of plasma angiotensin II (Ang II) levels in both strains was also observed. Strikingly, trained SHR, but not trained Wistar rats, showed a twofold increase in left ventricular Ang(1–7) levels. No significant changes were observed in plasma Ang(1–7) and left ventricular Ang II concentrations in either strain. Furthermore, Mas mRNA and protein expression in left ventricle were substantially increased in trained SHR. The physical training protocol used did not change blood pressure in either strain. These results suggest that the beneficial effects induced by swimming training in hypertensive rats might include an augmentation of Ang(1–7) and its receptor in the heart. (Received 6 November 2007; accepted after revision 7 February 2008; first published online 15 February 2008) Corresponding author: R. A. S. Santos: Department of Physiology and Biophysics, Avenida Antˆ onio Carlos, 6627-ICB- UFMG, 31270-901 Belo Horizonte, MG, Brazil. Email: marrob@ciclope.Lcc.ufmg.br Clinical and experimental data have indicated a beneficial effect of physical training on cardiovascular function in both normotensive and hypertensive humans and other mammals (Cox et al. 1985; Schaible & Scheuer, 1985, 1986; Friberg et al. 1988; Geenen et al. 1988; Negr˜ ao et al. 1992). Although the precise mechanisms by which exercise ameliorates cardiovascular function are not fully understood, putative factors include increased myocardial contractility (Schaible & Scheuer, 1985), improved myosin ATPase activity (Schaible et al. 1986), improved systolic heart function (Schaible et al. 1986), decreased myocardial oxygen consumption (Friberg et al. 1988), elevation of stroke volume (Friberg et al. 1988), and reduction of resting (Geenen et al. 1988; Negr˜ ao et al. 1992) and submaximal heart rate (Cox et al. 1985). Accordingly, physical training reduced ventricular failure induced by hypertension (Moreno J ´ unior et al. 1995), recovered ATPase activity and improved systolic function in spontaneously hypertensive rats (SHR) subjected to swimming training (Scheuer et al. 1982). It has been suggested that a decreased plasma renin activity is also involved in the beneficial effects of physical training in SHR (Hayashi et al. 2000; Zamo et al. 2004) and in humans (Geyssant et al. 1981). Furthermore, exercise training decreased plasma angiotensin (Ang) II levels in humans with chronic heart failure (Braith et al. 1999). Although Ang II is the major effector of the renin– angiotensin system (RAS), various other angiotensins are now recognized as being biologically active. Angiotensin(1–7) is considered to be an important peptide fragment of the RAS because it has important actions which are often opposite to those of Ang II. Several C  2008 The Authors. Journal compilation C  2008 The Physiological Society DOI: 10.1113/expphysiol.2007.014293