Figure 1
Baseline values of mean arterial pressure (MAP, A) and heart rate (HR, B) of anesthetized normotensive (SHAM, n=5−8) and hypertensive (2K1C, n=5−8) rats, either sedentary (SED) or subjected to physical exercise training (Ex), after 2, 4, 6, 8, and 10 weeks of swimming. *P<0.05 compared to SHAM SED rats. #P<0.05 compared to 2K1C SED rats (two-way ANOVA followed by Bonferroni test).
Figure 2
Index of the sensitivity of baroreflex bradycardia (ms/mmHg) induced by injection of phenylephrine (4.0 mg, iv) in normotensive (SHAM, n=5−8) and hypertensive rats (2K1C, n=5−8), either sedentary (SED) or subjected to physical exercise training (Ex), at 2 (A), 4 (B), 6 (C), 8 (D), and 10 weeks (E) of swimming. *P<0.05 compared to SHAM SED rats. #P<0.05 compared to 2K1C SED rats (two-way ANOVA followed by Bonferroni test).
Figure 3
Cardiomyocyte diameter (µm, A), number of myocardial inflammatory cells per microscopic field (B), myocardial collagen deposition (µm2/microscopic field, C), and left ventricle wall thickness/lumen ratio (Wt/L, D) of normotensive (SHAM, n=3−7) and hypertensive (2K1C, n=3−5) rats, either sedentary (SED) or subjected to physical exercise training (Ex), for 2, 4, 6, 8, and 10 weeks of swimming. *P<0.05 compared to SHAM SED rats. #P<0.05 compared to 2K1C SED rats (two-way ANOVA followed by Bonferroni test).
Figure 4
Photomicrographs of the myocardium of normotensive (SHAM) and hypertensive (2K1C) rats, either sedentary (SED) or subjected to physical exercise training (Ex, swimming) for 4 and 8 weeks. The number of inflammatory cells is consistent with the framework of normality in SHAM SED rats (A and C). The number of inflammatory cells (black arrows) is increased in SHAM Ex (E and G), 2K1C SED (I and K), and 2K1C Ex rats (M and O). The area with collagen deposition is compatible with normality in SHAM SED rats (B and D). Note the large area of collagen deposition (white arrows) in 2K1C rats (J and L) and small area of collagen deposition, similar to the normal pattern of SHAM SED rats, in 2K1C Ex rats (N and P). A, E, I, M, C, G, K, and O are stained with hematoxylin and eosin. B, F, J, N, D, H, L, and P are stained with Masson trichrome. All photomicrographs are magnified to 440× (bar=25 µm).
Figure 5
A and C, number of inflammatory cells per microscopic field in left (clipped) and right (non-clipped) kidneys, respectively. B and D, collagen deposition (µm2/microscopic field) in left and right kidneys, respectively, of normotensive (SHAM, n=3−6) and hypertensive (2K1C, n=3−5) rats, either sedentary (SED) or subjected to physical exercise training (Ex), for 2, 4, 6, 8, and 10 weeks of swimming. *P<0.05 compared to SHAM SED rats. #P<0.05 compared to 2K1C SED rats (two-way ANOVA followed by Bonferroni test).
Figure 6
Photomicrographs of the left kidney of normotensive (SHAM) rats and hypertensive (2K1C) rats, either sedentary (SED) or subjected to physical exercise training (Ex, swimming) for 4 and 8 weeks. The number of inflammatory cells is consistent with the framework of normality in SHAM SED rats (A and C). The inflammatory process (black arrows) observed in the left kidney in SHAM Ex rats at week 8 (G), 2K1C SED rats (I and K), and 2K1C Ex rats (M and O) is similar to the normal pattern observed in SHAM SED rats. Note the area with collagen deposition compatible with normality in SHAM SED rats (B and D). Note the large area of collagen deposition (white arrows) in 2K1C rats (J and L) and small area of collagen deposition in 2K1C Ex rats at week 4 (N); however, at week 8, the area of collagen deposition in 2K1C Ex rats resembled the normal pattern of SHAM SED rats (P). A, E, I, M, C, G, K, and O are stained with hematoxylin and eosin. B, F, J, N, D, H, L, and P are stained with Masson trichrome. All photomicrographs are magnified to 440× (bar=25 µm).
Figure 7
Photomicrographs of the right kidney of normotensive (SHAM) rats and hypertensive (2K1C) rats, either sedentary (SED) or subjected to physical exercise training (Ex, swimming) for 4 and 8 weeks. The number of inflammatory cells is consistent with the framework of normality in SHAM SED rats (A and C, respectively). The number of inflammatory cells decreased in SHAM Ex rats at week 4 (E) and in 2K1C Ex rats at week 4 (M). The inflammatory process (black arrows) observed in the right kidney in SHAM Ex rats at week 8 (G), 2K1C SED rats (I and K), and 2K1C Ex rats (M and O) was similar to the normal pattern observed in SHAM SED rats. Note the area of collagen deposition compatible with normality in SHAM SED rats (B and D). Note the large area of collagen deposition (white arrows) in 2K1C rats (J and L) and small area of collagen deposition in 2K1C Ex rats (N and P). A, E, I, M, C, G, K, and O are stained with hematoxylin and eosin. B, F, J, N, D, H, L, and P are stained with Masson trichrome. All photomicrographs are magnified to 440× (bar=25 µm).
Figure 8
Relative level of TBARS, reported as malondialdehyde equivalents (U/mg protein), in the left ventricle (A and B), left kidney (C and D), and right kidney (E and F) of normotensive (SHAM, n=10) and hypertensive (2K1C, n=10) rats, either sedentary (SED) or subjected to 4 or 8 weeks of physical exercise training (Ex). *P<0.05 compared to SHAM SED. #P<0.05 compared to 2K1C SED (ANOVA followed by Bonferroni test).
Figure 9
Catalase activity (U/mg protein) in the left ventricle (A and B), left kidney (C and D), and right kidney (E and F) of normotensive (SHAM, n=10) and hypertensive (2K1C, n=10) rats, either sedentary (SED) or subjected to 4 or 8 weeks of physical exercise training (Ex). *P<0.05 compared to SHAM SED group. #P<0.05 compared to 2K1C SED (ANOVA followed by Bonferroni test).