Abstract

Exercise training (Ex) has anti-hypertensive and renal protective effects. Renin-angiotensin system (RAS) are involved in the regulation of blood pressure and renal damage. In this study, we investigated the effects of the Ex on renal RAS in Dahl salt-sensitive rats. Six-week-old, male Dahl salt-sensitive rats were divided into four groups: 1) normal salt diet (NS); 2) NS + Ex; 3) high salt diet (HS); 4) HS+ Ex. NS or HS groups were fed diet containing 0.6% or 8% NaCl, and treadmill running was performed in Ex groups for 8 weeks (5 days/week; 60 min/day at 16-20 m/min, 0% grade). Systolic blood pressure (SBP) was monitored by tail-cuff method. Urine samples were collected on ice for 24 hours with metabolic cage. After 8 weeks, protein expression of RAS components in renal cortex (CO) and outer medulla (OM) were investigated by Western blotting. HS significantly elevated SBP (209±6 vs. 114±3 mmHg), and Ex did not change SBP (205±8 mmHg). HS significantly decreased creatinine clearance (0.96±0.04 vs. 2.57±0.07 ml/min/g kidney weight), but Ex significantly mitigated creatinine clearance (1.35±0.18 ml/min/g kidney weight). HS significantly increased urinary protein excretion (433±37 vs. 16±2 mg/day), but Ex significantly suppressed urinary protein excretion (327±22 mg/day). HS induced glomerular sclerosis, but Ex suppressed it. HS increased angiotensinogen expression (138 % and 328 %) and decreased renin expression (47% and 24%) in the CO and OM. HS increased angiotensin II type 1 (AT1) receptor expression in the OM (149%) and Mas receptor expression in the CO (198%), but decreased angiotensin II type 2 (AT2) receptor expression in the CO and OM (53% and 36%) and Mas receptor expression in the OM (20%). Ex improved HS-increased angiotensinogen and AT1 receptor expressions only in the OM. Ex improved HS-decreased renin expression in the CO and OM, and HS-decreased AT2 and Mas receptor expressions only in the OM. These results indicated that Ex improves HS-induced renal damage independently of SBP with specific changes of RAS components in the OM. Ex may have beneficial effects in HS-induced renal damage.

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