Oliveira Edilamar M, Sasaki Maurício S, Cerêncio Marcela, Baraúna Valério G, Krieger José E
Laboratory of Biochemistry, School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil.
J Renin Angiotensin Aldosterone Syst. 2009 Mar;10(1):15-23. doi: 10.1177/1470320309102304.
This study addressed the role of the local renin-angiotensin system (RAS) in the left ventricular hypertrophy (LVH) induced by swimming training using pharmacological blockade.
Female Wistar rats treated with enalapril maleate (60 mg.kg(-1).d( -1), n=38), losartan (20 mg.kg(-1).d(-1), n=36) or high salt diet (1% NaCl, n=38) were trained by two protocols (T1: 60-min swimming session, 5 days per week for 10 weeks and T2: the same T1 protocol until the 8(th) week, then 9(th) week they trained twice a day and 10(th) week they trained three times a day). Salt loading prevented activation of the systemic RAS. Haemodynamic parameters, soleus citrate synthase (SCS) activity and LVH (left ventricular/body weight ratio, mg/g) were evaluated.
Resting heart rate decreased in all trained groups. SCS activity increased 41% and 106% in T1 andT2 groups, respectively. LVH was 20% and 30% in T1 andT2 groups, respectively. Enalapril prevented 39% of the LVH in T2 group (p<0.05). Losartan prevented 41% in T1 and 50% inT2 (p<0.05) of the LVH in trained groups. Plasma renin activity (PRA) was inhibited in all salt groups and it was increased in T2 group.
These data provide evidence that the physiological LVH induced by swimming training is regulated by local RAS independent from the systemic, because the hypertrophic response was maintained even when PRA was inhibited by chronic salt loading. However, other systems can contribute to this process.
本研究通过药物阻断探讨了局部肾素 - 血管紧张素系统（RAS）在游泳训练诱导的左心室肥厚（LVH）中的作用。
用马来酸依那普利（60 mg·kg⁻¹·d⁻¹，n = 38）、氯沙坦（20 mg·kg⁻¹·d⁻¹，n = 36）或高盐饮食（1% NaCl，n = 38）处理的雌性Wistar大鼠，通过两种方案进行训练（T1：60分钟游泳时段，每周5天，共10周；T2：与T1方案相同至第8周，然后第9周每天训练两次，第10周每天训练三次）。盐负荷可防止全身RAS的激活。评估血流动力学参数、比目鱼肌柠檬酸合酶（SCS）活性和LVH（左心室/体重比，mg/g）。
所有训练组的静息心率均下降。T1组和T2组的SCS活性分别增加了41%和106%。T1组和T2组的LVH分别为20%和30%。依那普利可预防T2组39%的LVH（p<0.05）。氯沙坦可预防训练组T1中41%和T2中50%的LVH（p<0.05）。所有盐组的血浆肾素活性（PRA）均受到抑制，但T2组的PRA升高。
这些数据表明，游泳训练诱导的生理性LVH由独立于全身的局部RAS调节，因为即使慢性盐负荷抑制PRA时肥厚反应仍持续存在。然而，其他系统也可能参与此过程。
