Exercise training maintains cardiac output and stroke volume in hypertensive TG (mREN‐2)27 rats with impaired diastolic function

Abstract

The role of the renin-angiotensin system (RAS) on in vivo cardiac function, blood pressure, and markers of maladaptive cardiac hypertrophy were determined after low-intensity exercise training (ET) in Ren-2 rats and age-matched Sprague Dawley (SD) controls (3–4 weeks). After 5 weeks of treadmill ET, echocardiography demonstrated that both cardiac output (ml / min) and stroke volume (ml) per body weight (g) were increased (p<0.05) by ET in both SD and Ren-2. The slope of mitral deceleration time (m/sec2), a non-invasive measure of diastolic function, was lower in the Ren-2 rats, but not changed by ET in either rat strain (p>0.05). Systolic, diastolic, and mean (MAP) blood pressures via tail-cuff method in Ren-2 rats were higher compared to the SD controls, while ET had no effect. LV collagen deposition, as assessed by hydroxyproline assay, was not affected by rat strain or ET. B-type natriuretic peptide (BNP) mRNA levels measured in the left ventricle (LV) by real-time PCR were higher in the Ren-2 rats (100%), but not affected by ET (p=0.81). Both α (~14.5 fold) and β (~2.5 fold) myosin heavy chain mRNA were higher in the LV of Ren-2 rats compared to SD (p < 0.05), but were not changed by ET. These data suggest that ET restores cardiac index and stroke volume in the Ren-2 rat.